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722 Cards in this Set
- Front
- Back
Properties of AP?
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1. big/fast; 2. All or none; 3. Invariant; 4. Conducted rapidly; 5. Refractory period
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Ion direction with NA+/K+ pump?
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2 Na+ is pumped out, 3 K+ is pumped in
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EPSP definition?
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Excitatory post synaptic potential—the depolarization that the dendritic spine undergoes (passive spread/depolarization)
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What is responsible for all or none AP?
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The presence of voltage gated Na+ channels at the axon hillock
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Draw a simple reflex and describe mediators
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1. muscle spindle senses increased tension; 2. Afferent info travels to SC; 3. Synapses and feeds back to muscle of interest to increase tension
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Define divergence
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A sensory neuron may get info from multiple spindles (multiple specialized sensory regions), but feed to one neuron
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Define convergence
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Multiple sensory fibers impacting a single motor neuron
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What does the resting memb. potential represent
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The RMP represents a separation of charge that is maintained through the action of the Na+/K+ ATPase via active pumping of Na+ out and K+ in
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AP characteristics?
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~1 ms; 0.1 volt amplitude; overshoot (because Na+ closed and K+ open [cell goes to K+ equilibrium]; all or none
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How are duration and intensity of stretch encoded?
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Duration of stretch= duration of AP “train”
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Draw the relationship (time and intensity) as described above
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What causes the relative refractory period? How long?
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Caused by increased K+ conductance, fact that some Na+ channels still have a “ball” blocking the hole; usually <5 ms, but 1-10 ms is the range
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What mediates absolute ref period?
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Mediated by “ball” [ball and chain model] that blocks the channel; this makes sure AP’s don’t travel in both directions
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Draw and exp. temporal summation
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Temp. sum. is a result of the lack of IMMEDIATE voltage dissipation within the cell dotted line = threshold
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Exp. spatial summation
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Cell gets multiple input from axons at same time, these sum at the axon hillock, but come from spatially distinct dendrites
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IPSP
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Inhbitory post synaptic potential; usually used Cl- to “buffer” a cell from reaching threshold
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Properties of local potentials
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1. graded [not AP]; 2. Travel passively; 3. Dissipate quickly
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What does Nernst eq. do?
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Describes the voltage across the membrane in terms of K+
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What is happening with ions in equilibri
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There is no net movement of charge
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What are general bits of info re: [ions] in/out & voltage.. don’t memorize
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Ion Out In Eq. Pot.
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Most cells selectively perm to what?
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K+; they have a straight curve for [K+] vs. rest mem potential
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What determines the rest mem potential?
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The ion concentrations and the charges on each side of the membrane = electrochemical equilibrium
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Does the [ion] change much?
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NO; it is mostly charge that moves when the membrane depolarizes not a significant number of ions
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How much (%) can Na/K ATPase use?
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Incredible amounts 60-80% of some neurons needs, this now makes sense that even resting the brain uses 20% of O2
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Draw the difference in membrane potential vs. [K+] for both glia and neurons; why does this happen (in general)
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the cell is also permeable to Na+
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What is the Goldman equation; how is it different from Nernst
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Goldman takes into account multiple ions, Nernst is generally set up only to take into consideration K+
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Why is an EPSP depolarizing?
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The action of neurotransmitter opens Na+ channels which move down both electrical and chem. gradient into cell
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What are the 4 main characteristics of AP?
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1. all or none; 2. Threshold for AP generation; 3. Refractory period; 4. The AP doesn’t dissipate with increasing distance
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Why is there an AP threshold at all? What range is considered to be threshold?
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There is a threshold because the Na+ channels are voltage sensitive [probability of being open depends on increasing voltage]; therefore if you hit a certain depolarization a positive feedback loop gets started and creates the all or none AP. –(-40)→(-30) mV is threshold
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This is one of the most important things you will learn… Why does the AP initially decrease?
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Volatage of the membrane (dotted) rises initially because permeability to Na+ has increased (gNa+); then the slower K+ voltage channels open and bring charge out of cell (down electrical and chemical gradient)… Later, all the Na+ channels are stuck inactivated via “ball-and-chain” which allows overshoot
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What are the slower K+ channels called?
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Delayed-rectifying potassium channels (due to their 1 msec delay in opening in response to the voltage change)
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Which channel type primarily determines the AP of a cell?
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The K+ channels, because they are the ones responsible for repolarization; e.g. is the cardiac calcium-dependent Ca++ channel diagramed here
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What do TTX and STX block?
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TTX- Tetrodotoxin & STX- saxotoxin both block Na+ channels
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What are the toxins that block K+? Who cares?
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TEA- tetraethylammonium; 4-AP- 4- aminopyridine; these have been useful to determine membrane properties via examination of a single type of ion channel
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How do local anesthetics work? Antitiarrythmics?
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e.g. lidocaine works by blocking the Na+ channels, can also decrease cardiac excitability
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How does voltage normally spread down a conduit? Why need APs?
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Normally voltage spreads passively and degrades quite quickly; therefore APs (and nodes of Ranvier) re-generate the AP to allow quick, non-degrading spread of information
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What is the length constant? Why care?
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Tau (when current injected has degraded to 37%); it is mostly useful to compare cells ability to spread current; a length constant is <1 mm; therefore you need AP to communicate long distance
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Why does the AP travel in only one direction?
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This is because of the absolute (and relative) refractory period that is generated “behind” the AP due to the “ball-and-chain” model of inactivation of voltage sensitive Na+ channels
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What is the node spacing in myeliniated axons?
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Nodes are about 100 times the diameter of the axon; he said in the syllabus that it was interstingly “optimal” – this isn’t interesting… the ones that weren’t optimal were eaten by tigers (too bad). The signaling required to optimize is interesting
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What is hyperkalemic periodic paralysis?
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“ball-and-chain” is damaged; therefore patient uses up all ATP then collapses to the floor
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What are the main kinds of neuronal connections?
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1.
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2.
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Minor- Electrical- fast, invariant response
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How is NT released?
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In “quanta” essentially vesicles – although new research shows that some areas have “kiss-and-run” therefore non-quantal release
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What is a MEPP?
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Miniature end plate potential; it is the depolarization from the release of one (or a few) vesicles of NT
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What are characteristics of Lambert-Eaton
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1. pts produce Ab agains P/Q voltage sensitive Ca++ channels in axon terminal; 2. Therefore low levels of VGCa++ Channels in terminal- this causes insufficient Ca++ entry and limited vesicular release; 3. Associated with carcinoma (… for some reason the carcinoma activates immune system to self)
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How to vesicles release contents? Who cares?
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V & T-snare hypothesis; Ca++ allows the binding, capture, and release of NT within vesicles.
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Why does Lambert-Eaton show a U shaped curve
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because there is a slow accumulation of Ca++ in the synaptic buton allowing more vesicles to release contents [this is called facilitation]
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What is the omega profile?
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It is the EM pic of a vesicle fused (very illustrative)
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What happens at buton for NT release?
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1. AP travels down axon; 2. Volt sense Ca++ channels open; 3. Vesicle fuses through V&T-snares; 4. NT released into cleft
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How is [Ca++] decreased in buton?
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Via possible mitochondrial buffering; Ca++ pumping out of buton
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What are the actual proteins in V&T snare hypothesis?
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V-Snares→ synaptobrevin
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What would increased [Ca++] do to vesicle release?
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The increased [Ca++] would tend to increase the vesicular release because it is required for snare binding
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Where are places where kiss and run happens
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The retina is a place where quantal release does not happen always (specifically the rods and cones)
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How does botox work?
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Botox is a zinc endopeptidase (there are multiple) that is targeted to some component of the NMJ (there are also multiple targets)
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What are some characteristics of NT?
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1. synthesized and concentrated in neurons; 2. Released from neurons; 3. Local application mimics synaptic release; 4. There are mechanisms for removal of protein
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Where is ACh mainly found?
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it is the main NT at the neuromuscular junction, it is also used in the basal forebrain
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What NT is inhibitory?
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The main inhibitor in the brain in GABA (amino acid)
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What NT are in the monoamine class? Function?
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dopamine; 2. Serotonin; 3. Norepi; 4. Epi; 5. Histamine→ these are all based off the tryptophan & tyrosine; -----Function→ modulation of other NT
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What do the peptide NT do?
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Conrol hypothalamic pituitary axis; feeding/sexual behavior
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Where are NT released?
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from the synaptic buton; in quanta (usually); in an active zone (can be seen on EM)
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How is NT loaded into cells?
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H+ ATPase on surface of vesicle pumps H+ in; this H+ is allowed to exit through a co-transporter and NT gets to come in
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What is the rate limiting step in Catecholamine syn? Who cares?
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Tyrosine hydroxylase is the rate limiting step; this is only important because knowing some rate limiting steps allows you to know places to intervene to increase or decrease amount
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What are the Catecholamines?
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Tyrosine→ L-Dopa→ Dopamine→ Norepinephrine→ Epinephrine
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What are the fates for dopamine
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1. degradation by COMT/MAO; 2. Reuptake and degradation; 3. Reuptake and repackaging
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How is cocaine thought to work?
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Through the inhibition of dopamine transport (therefore there is increased dopamine in the cleft)
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How are Amphetamines thought to work?
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Crank, X (works same way); disrupt proton gradient allowing NT leakage (not through vesicle fusing)
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clinical ways to increase dopamine?
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L-Dopa (precursor); MAOi (monoamine oxidase inhibitor); COMT
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ACh degraded how?
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AChE; choline take into buton; combined with Aceyl CoA= ACh
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How do VX and Sarin gas work?
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They inactivate AChE, this causes too much ACh in the cleft and paralysis (because you run out of ATP)
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How is glutamate recycled?
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Glutamate uptake into glia; converted to glutamine; shuttled to neurons and made back into glutamate
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How are Neuropeptides made?
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They are proteins; therefore made in ER→ Golgi→ endosomes → released; because a protein must be resynthesized
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What are brisk reflexes indicative of?
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Upper motor neuron damage; long term this has increased tone; together this is termed spacticity
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What would getting knifed in the back give you?
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1. A very bad day; 2. Brown-Sequard syndrome: ispilesional weakness, loss of Big 4; contralateral loss of little 3
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Drawbacks & good of electrical synapses?
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1. no amplification is possible; 2. Cell sizes matter (usually cells are same size)… Good → fast; bi-directional
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2 main classes of a chemical synapse
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1. directly gated/coupled (receptor for NT and channel in same protein); 2. Indirectly gated/coupled→ GPCR (usually)
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Benefits of indirect coupling?
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1. allows for massive amplification; 2. Allows for changes in gene expression; 3. Allows multiple signals to converge
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What causes Myasthenia Gravis?
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Immune reaction against the AChReceptors (causing endocytosis)
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What are the two main drug classes for seizures? Function?
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1. Diazepams→ act as GABA agonists (increasing inhibition); 2. Valproate→ increases GABA synthesis
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Define direct coupling
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NT receptor and channel are part of the same complex
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Inhibitory synapses included which ions?
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Mainly Cl- and K+ because both tend to polarize cell (move cell further from threshold)
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Can inhibitory signals depolarize the cell?
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Yes; the cell can get closer to the threshold, but they “clamp” the cell and still make it harder for Na+ to bring to threshold
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What does Succinyl choline do? Why?
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Flaccid paralysis; this is because it keeps ACh like action in the cleft for a long time, this desensitizes the NMJ
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Best plasticity catch phrase?
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“Fire together wire together”
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How do we think memory is formed [generally]
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We think that long term potentiation & depression (LTP/D) forms the basis for the changes in weighting given to neurons
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What’s the difference between AMPA and NMDA receptors?
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Both respond to glutamate; has Mg++ in the pore (which is kicked out by high depolarization) allowing Ca++ to enter cell; this high Ca++ causes changes in gene expression→ magic→ LTP (Note: Ca++ is also required for LTP).
NMDAR activation along with AMPAR activation can result in LTPotentiation. |
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What does Ca++ do?
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Ca++ activateds CaMKII (which can phosphorylate lots of stuff); KO mice lack LTP; loading a cell with CaMKII mimics LTP
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What is the end result of this stuff?
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More AMPA receptors are expressed at the surface; therefore higher depolarization with each incoming signal
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Differences between LTP/D?
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high frequency vs. low frequency stimulation
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Describe Hippocampus pathway
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1. perforant pathway contact granual cells; 2. Granual cells contact CA3 pyramidal cells (which send out axons as schaffer collaterals); 3. These SC synapse with CA1
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What are the main divisions of PNS
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1. sensory; 2. Motor; 3. Autonomic (which is divided into sympathetic and parasympathetic)
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Bundles of nerves are called?
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fasicles
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Draw the parts of the nerve bundles and label
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Epineurium- most outside tough—collagen and epithelial cells)
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How do PNS axons grow back? Speed?
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Through the sheath that remains used for guidance; grow back about 1 mm/day
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Where are sensory neuron cell bodies
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DRG
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Number and division of SC roots
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31 roots; 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal
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How are mechano-receptors specialized?
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They can be specialized to detect vibration, light touch, temp, chemicals, pain→ this is accomplished via the end organ
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What do propioceptors do?
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they bring fine motor information re: limb and muscle position
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What are muscle spindles? Do?
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specialized muscle cells (intrafusal) that wrap sensory axons; they contract and stretch to keep receptor sensitive;
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What are the two kinds of MS fibers? Info conveyed by?
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Nuclear chain- provide static info about length- IIa
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What are reflex arcs good for?
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1. coordinating movements; 2. (more importantly?) maintaining static position
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why …CNS damage cause hyperreflexia?
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The stretch reflexes are inhibitied via a connection from the CNS, if this inhibition is lifted the reflexes are enhanced
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channels that underly temp sense?
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TRP channels; have temp sensitive Na+ channels, these channels also respond to chemicals (e.g. capsacin)
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What are the two separate pain fibers?
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A delta- small myelinated carry fast info
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What is in a motor unit?
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1. motor neuron; 2. NMJ; 3. At least one muscle fiber (the units get smaller for fine control-e.g. eyes)
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Review muscle contraction
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Smooth muscle contraction
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1. depolarization; 2. Ca2+ influx through L-type volt sense Ca2+ channel; 3. Tyanodine receptor binding; 4. Ca2+ release; 5. Ca2+ binds calmodulin and activates light chain kinase (thus phosphorylating myosin and causing APTase activity of myosin)
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ANS divisions and functions
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Symp- fight or flight- ACh then noreipi
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Which axon for both para/ sympathetic is the longer one? Who cares?
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→The sympathetic preganglionic axon is short (top)
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What does symp stim do to iris, salivary, sweat, bronchi, heart, GI, sex organs, bladder
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Syptathetic stimulation dialates the iris, decreases salivation, increases sweatin, dilates bronchi, increases HR, decreases GI motility, constricts vasculature (aroused state), constrict bladder sphincter & relax detrusor
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How does caffeine work?
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antagonizes adenosine A1 receptor thereby increasing norepi release in the PNS and CNS
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What is the NT for para sympathetic?
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ACh only (pre & post ganglionic); remember ganglia are usually embedded in tissue
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Enteric NS (ENS)
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Controls the function of the GI, it really is the bastard stepchild and gets no attention; it has the machinery to function separate from the CNS
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What are some characteristics of Charcot-Marie-Tooth?
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1. both sensory and motor function loss; 2. Classical “claw-like” hand posture; 3. Caused by demylination of PNS; 4. Mutation in connexin 32 (which are needed for gap junctions)
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Guillan Barre Syntrome
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GBS- rare autoimmune reaction (following URI or vaccination); sudden loss of both sensory and motor control; extensive supportive care is needed (as is immunosupression)
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Ulnar nerve palsy
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leaning on ulnar nerve (can been seen in alcoholics)
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what (specifically) provides a conduit for PNS regeneration?
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the perineurium, epineurium, and endoneurium; therefore surgical repair requires accurate aposition
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What myelinates PNS? Derived from?
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Schwann cells myelinate PNS; NCS derived, each Schwann myelinates only a single (portion) axon
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What is EMG and Nerve conduction used for?
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These measure speed of conduction, and also are a surrogate for the number of axons conveying information
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What covers the SC?
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The three layers of meninges; 1. Pia; 2. Arachnoid; 3. Dura
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# of spinal nerves from each segment?
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2 (remember bilateral)
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Gestalt of Big 4 path
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1. DRG gracile cunate fasiculi; 2. G & C nuclei; 3. Thal VPL
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Gestalt of little 3
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1. DRG neuron; 2. Synapse dorsal horn, cross in anterior white commisure; 3. VPL in thal to cortex
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Gestalt of CST (cortico-spinal)
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cortex, synapes with LMN in layer #9, out to muscle
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where does the SC end, where LP done?
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SC ends around L1/2; and LP is done @ L4/5 (in the lumbar cistern)
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draw each of the tracts and synapses, label neuron number
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DCML path neurons # and function
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1st cell body in DRG, synapses in G & C nuclei; 2nd G & C nuclei to the VPL thal; 3rd thalamus to the cortex
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Differences between spinothal & DCML?
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is in the 2nd order neuron location DCML is in the G & C nuclei, whereas the Spinothal synapses after going up or down a little
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annoying but important… layers and functions of SC areas… Draw
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What are Lamina I/ II?
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Marginal zone (I) Substantia gelatinosa (2) many spinothalamic 2nd order nerons have CB here
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What are Lamina III-VI doing?
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Nucleus proprius (forms the majority of the dorsal horn) processes sensory info (discussed later)
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Lamina VII
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Clarke’s nucleus between C8 –L2
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Lamina IX
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ventral horn motor neurons
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Lamina X
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periaqueductal grey- thought to do “something” with pain
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Again what is Brown-Sequard syndrome
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Hemisection of SC causing loss of Big 4 contralateral and little 3 ipsilateral; paralysis on side of section
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What are Betz cells? Where are they?
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Betz cells are in layer V of the cortex, they are the pyramidal cells that synapse in the ventral horn for motor action ( their axons forms most of cotricospinal tract) 90% cross at pyramids
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Signs of UMN damage
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hyper-reflexia and increased tone (from lack of inhibition)
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signs of LMN disease
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muscle wasting (chronic) hypo-reflexia, flaccid
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Draw and describe 4 main functional components of spinal nerves
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GSA- general somatic afferent- sensory BIG 4 & little 3
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Draw the circle of willis, describe what each vessel feeds
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occlude an ICA what happens?
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Generally nothing, that is why you have a circle of willis
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what is supplied by posterior circ?
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Brainstem, pons, occipital lobes (generally), and thalamus; infarction of the thalamus can mimic hemispheric MCA stroke
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Draw the circle again
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What are the most common branches for stroke
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The lenticulostriate areteries these feed the basal ganglia and the internal capsule
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Describe that path of the cartotid to M1 branch
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1. through carotid canal; 2. Curves while within the cavernous sinus; 3. Penetrates the dura; 4. Ophthalmic branches while still ICA; 5. Then MCA & ACA separate
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Describe M1 MCA→ distal braches course
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M1 MCA then either bifurcates or trifurcates; 2. Travels over the insula; 3. Within the sylvian fissure; 4. Then most of the lateral surface of the brain
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Describe the posterior circ branches and what they come off
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1. posterior spinal- come of each vert; 2. Anterior spinal join, but come off each vert; 3. PICA comes off each vert… can come off at different levels (L & R); 4. AICA off basilar; 5. SCA (smaller just under PCA off basilar); 6. PCAs (normally); 7. Thalamoperforating arteries
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Thing to remember when describing vasculature
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IT IS VARIABLE!! Not everyone has a complete circle, not every one has PCA’s that come off the Basilar, not everyone’s territory of perfusion is the same for each vessel
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What is unusual about brain veins?
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not usually with arteries, they don’t have valves
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Draw and label venous flow
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Basic concepts re: brain metabolism?
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Brain is hungy: 20% glucose, possibly 50% oxygen (resting requirements); <60 sec after blood flow stops unconscious
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How is cerebral blood flow maintained with changes in BP?
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Through autoregulation: therefore increases in BP don’t change tissue perfusion
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Describe they types of hemorrhages and causes
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Epidural- often from trauma, minndle meningeal aretery tears
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Draw and label ventricles (figure →)
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This is a great figure. Notice how anterior and posterior the horns traverse
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What is within the vents making CSF?
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Choroid plexus (yucky crappy looking stuff in dissection)
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Describe the flow of CSF
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1. lateral vents; 2. Foramen of monro; 3. 3rd Vent; 4. Cerebral aqueduct; 5. 4th vent; 6. Out foramen luschka (lateral) & magendie (medial); 7. Into subarachnoid space (around all CNS essentially); 8. Arachnoid villi; 9. Sup sag sinus; 10. I Jug
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Cisterns of brain: what are they? What are a few? draw
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They are enlargements in the space for CSF
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Characteristics of normal CSF? function
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clear, colorless, odorless; functions to support brain (so it floats… 1400 gram brain weighs 50 grams while floating)
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Rate CSF made; amount of CSF in brain
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CSF is made about 20 cc/hr, but total CSF is only 150 cc; therefore it must be reabsorbed or the stupid choroids plexus keeps making and you get hyrocephalus
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Types of hydro
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1.
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2.
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non-communicating usually obstruction of aqueduct or other small communication
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Draw and label ventricles (figure →)
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This is a great figure. Notice how anterior and posterior the horns traverse
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What is within the vents making CSF?
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Choroid plexus (yucky crappy looking stuff in dissection)
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Describe the flow of CSF
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1. lateral vents; 2. Foramen of monro; 3. 3rd Vent; 4. Cerebral aqueduct; 5. 4th vent; 6. Out foramen luschka (lateral) & magendie (medial); 7. Into subarachnoid space (around all CNS essentially); 8. Arachnoid villi; 9. Sup sag sinus; 10. I Jug
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Cisterns of brain: what are they? What are a few? draw
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They are enlargements in the space for CSF
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Characteristics of normal CSF? function
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clear, colorless, odorless; functions to support brain (so it floats… 1400 gram brain weighs 50 grams while floating)
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Rate CSF made; amount of CSF in brain
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CSF is made about 20 cc/hr, but total CSF is only 150 cc; therefore it must be reabsorbed or the stupid choroids plexus keeps making and you get hyrocephalus
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Types of hydro
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1.
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2.
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non-communicating usually obstruction of aqueduct or other small communication
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Big picture of BS
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Spinal cord like functions and integrative functions; 1. Acts as a conduit; 2. Gives rise to cranial nerves; 3. Integrative functions regulating respiration, cardiovascular and consciousness (via the reticular formation)
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What are two main reasons for unconsciousness? Differentiate?
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1.
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2.
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a lesion (possibly small) to the reticular formation
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What type of fibers arise from the Edinger westphal nuc
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Parasympathetic fibers to the iris, these fibers run with the third nerve; therefore with damage to the nerve or the nucleus you get a blown pupil (via release of parasympathetic drive)
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What are the 5th nerve nuclei/function
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Mesencephalic- propioception; Principal sensory- light touch; spinotrigeminal- pain and crude touch
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First things to do when identifying BS nuclei
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Which part of the brainstem? Is it medial (efferent) vs dorsolateral (afferent)
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Why unilateral facial droop?
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This is due to the fact that UMN were damaged, UMN for the forehead is bilateral, but face is only unilateral
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What should you always do to make sure a patient is dead
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You should check the “Dolls-Eyes” reflex→ eyes tend to stay back… dead they move with the head; Gag→ 9 in 10 out; corneal→ V2 in 7 out (blink)
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Nuclei in the pons?
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V-IIIV although 6-8 exit at the pontomedullary junction
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Which is the only nerve to exit dorsal
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The trochlear is the only nerve to exit dorsally, the trochlear also innervates the contralateral side
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What are & function of mixed nuclei
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V- facial sensation and mastication; VII- taste and 2/3 of tongue and facial expression; IX- Tase post 1/3 & swallowing; X- thoracic and abdominal viscera & speech, swallowing
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Pure sensory nuclei?
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1,2,8
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|
Pure motor nuclei
|
3,4,6,11 (head/shoulder),12 (tongue movements)
|
|
SSA & SVA
|
SSA- hearing, vision, balance; SVA- olfaction & taste
|
|
GSE
|
Derived from mesoderm (tongue [12] and extraocular muscles [3,4,6])
|
|
What are the rest of the muscles called?
|
Branchiomeric as they develop from the brachial arches—they are innervated by the SVE
|
|
SVE
|
Motor of V, Motor of VII, Nucleus ambiguous (9,10) [controls striated muscles of larynx and pharynx], accessory 11
|
|
GVE
|
Parasympathetic preganglionic neurons, E-W (3), superior and inferior salivitory nucleus (7,9) [salivation and mucous glands], motor of vagus [10] heart lung gut
|
|
Sensory include
|
GVA/SVA; SSA; GSA
|
|
GVA/SSA
|
Solitary nucleus (7,9,10)→carotid body, larynx, pharynx, heart, lungs, guts
|
|
SSA
|
Choclear nucleus (8), Vestibular (8)
|
|
GSA
|
V1-V3 for trigeminal, mesencephalic nucleus of 5 (propiorception of jaw); principal sensory of 5; spinal trigeminal nucleus → pain and temp for head & neck
|
|
Draw path of sense info to cortex from face
|
Principal sensory of 5, VMP thal, to cortex; pain via spinal V nucleus
|
|
Corticobulbar describes?
|
It describes the motor tract for the face and neck (that rely on BS neuclei)
|
|
|
VL-input BG (SNr GPi) CB; output to motor & premotor cortex
|
|
Relay nuclei of the sensory system
|
VPL- Body – DCML and spinothalamic output to sensory cortex
|
|
The only sense that doesn’t go to thal?
|
Olfaction goes directly to cortex
|
|
What are the parts of diencephalon and their parts
|
1. Epithalamus- pineal, habenular nuclei; 2. Subthalamus- STN functionally related to BG; 3. Hypothalamus- reg autonomic function and drive- behaviour
|
|
What are the main thal projections?
|
Diffuse projection nuclei, and relay nuclei
|
|
General principles
|
Connections with cortex are bi-directional; parallel info remains segregated in the thal e.g. pain light touch, joint postion in VPL
|
|
What is the internal medulary lamina?
|
It is a Y shaped band of white matter that divides the thal into three main sections: 1. Anterior; 2. Medial; 3. Lateral
|
|
Draw and label thalamic nuclei, if you want state the connections
|
|
|
VA & VL do?
|
Input from BG, output to motor/premotor cortex
|
|
VPM & VPL do?
|
Inputs from sense BIG 4 & little 3; outputs primary sensory
|
|
AV
|
Limbic fuctions: input from hypothal via mamilothalamic, output to the cingulated (emotion & memory?)
|
|
DM
|
Limbic functions: input amygdala, olfactory cortx, output prefrontal cortex (planning, organizing behavior)
|
|
Intralaminar nuclei
|
Input – BS reticular activating system, spinal cord; output- frontal cortex, other Thal nuclei (regulates alertness, consciousness?)
|
|
CM
|
Most prominent intralaminar nucleus
|
|
Reticular nucleus
|
Input- corticothalamic and thamocortical collaterals
|
|
What is thalamic pain syndrome?
|
After damage even light touch can stimulate strong feelings of pain
|
|
Pulvinar
|
Projects, connects lots of parietal and temporal association cortex
|
|
Lecture 15: Basal Ganglia
|
|
|
What is the nucleus accumbens
|
Anterior region where the head of the caudate and putamen join, part of reward center, think drug addiction
|
|
Why do we consider caudate and putamen one structure
|
They start as one structure, they have the same function (as far as we can tell) but during development they become separated by the internal capsule
|
|
Striatum=
|
Caudate + Putamen
|
|
SNc vs SNr
|
Pars compacta (SNc) vs Pars reticulata (SNr)
|
|
What is the function of SNc?
|
This is the modulatory part of the substantia nigra that contains dopamine. It increases movement likelihood in two ways: 1. Increasing signal to the direct; 2. Inhibiting the indirect
|
|
What is hemibalism? Cause?
|
It is uncontrolled movements of one side of the body; it is caused by STN damage
|
|
Damage in PD?
|
PD results from selective loss of neurons (dopamine containing) in the SNc → PD always think decreased movement (with rx)
|
|
Board question: what does the BG do?
|
“Gating of movements”
|
|
Draw the BG circuit
|
A circuit is diagramed below… use for reference
|
|
Who are the players in the BG circuit?
|
1. caudate; 2. Putamen; 3. GPe; 4. GPi; 5. STN; 6. SNr; 7. SNc
|
|
BG principal input/output?
|
Input- BG input from cortex to the caudate and putamen
|
|
What (on movement) does activity in GPi/SNr do?
|
Activity in these areas inhibits movement
|
|
Where do direct / indirect path go?
|
Direct- goes from caudate/putamen to GPi/SNr directly
|
|
What does the direct path do in general?
|
It inhibits the inhibitory output of BG; therefore it increases movement
|
|
What are hyperkinetic movement diseases?
|
HD- ultimately affects whole striatum, STN can’t be inhibited, so the inhibitory output (to stop movement) is inhibited so you get more movement
|
|
Pacinian corpuscle does?
|
Responds best to vibration & pressure
|
|
Meissner?
|
Responds to lower frequency vibration
|
|
What kind of info to slow adapting and fast adapting carry?
|
Slow adapting carry information (usually poor temporal resolution), but they tell you a stimulus is happening
|
|
What do Golgi tendon organs tell you?
|
They give you the tension that the muscle is under (they are hypothesized to stop (muscle) contracting if damage will occur
|
|
Joint receptors tell you?
|
The syllabus says propioception (I can tell you that is wrong [except possibly for knee])… unkown what it does… it might be a primative (reasonably unused) system for propioception
|
|
Anterolateral made of what?
|
The spinothalamic & spinoreticulothalamic; pain/temp/crude touch
|
|
How would you test the anterolateral sys?
|
You could do hot/cold and pain (e.g. pin-prick)
|
|
DC-ML?
|
BIG 4 from body (except head)
|
|
What is magnification re: brain tissue?
|
It is the ratio of cortex vs the area on the body (e.g. the lips have lots of cortex for size.. why you don’t kiss with you knees)
|
|
How does the DCML sharpen information?
|
Like vision there is excitatory center with inhibitory surround, therefore the inhibition allows greater sensitivity for the center, without this inhib you would have worse 2-point discrimination
|
|
Describe two-point discrimination over body surface?
|
Two point discrimination is very good in areas that have large cortical representations (better to think this way than innervation density) think skin vs back
|
|
Where does sensory info project?
|
Thalamic (VPL/M) info goes to the granule cells in layer 4; and to the dendrites of pyramidal cells in 3,5,6; output 5,6
|
|
Map in 3a for?
|
Most anterior for muscle afferents
|
|
3b
|
Slow and rapid adapting mechanoreceptors (aka fine touch)
|
|
1
|
Rapidly adapting neurons with slightly larger fields
|
|
Most posterior (2)
|
Receives input from joint afferents
|
|
How does a doctor assess pain in pts?
|
They really can’t; one must trust a patient… this is one reason that pain is such a huge problem
|
|
Is pain a good thing?
|
Acute paint is a warning (and useful); chronic pain is not
|
|
Is pain objective? And features?
|
No, it is not a stimulus→ “an experience”: components of pain actual stimulus, emotional, and cognitive
|
|
What is allodynia?
|
The perception of pain to normally non-painful stimuli
|
|
hyperalgesia
|
Increased sensitivity to pain
|
|
How does aspirin reduce pain?
|
|
|
What is the diff between nocioceptive and neuropathic pain
|
Nocioceptive- Pain produced from tissue injury (A-delta & C fibers); Neuropathic- from damage to the CNS (post herpes, phantom limb, thalamic pain syndrome) BURNING pain
|
|
Why do C & A-delta respond to noxious?
|
They generally have free nerve endings
|
|
Why pain with nerve compression?
|
The large fibers are the first to be KO and the nocioceptive small fibers are the last (remember cyanotic hand video)
|
|
Without large fibers how is pain perceived
|
All pain is perceived as burning in the absence of large fiber information
|
|
How do NSAIDs reduce pain
|
Inhibition of cyclooxygenase (which normally makes prostaglandins) and sensitizes nerve endings to pain
|
|
Back to SC Lamina
|
|
|
Lamina I; name? respond to?
|
Lamina I; marginal zone; responds to noxious stimuli; many cell bodies in this lamina contribute to spinothal tract
|
|
Lamina II; same drill as above
|
Lamina II; substantia gelatinosa; small interneurons, many respond to noxious stim; primary afferent from small fibers
|
|
Lamin III & IV
|
Respond to BIG 4, does not increase activity to noxious stim
|
|
Lamina V
|
Inhibitory and excitatory effects to non- noxious stim; also excited by noxious stim
|
|
Lamina VI
|
Respond to joint movements
|
|
Study the sensitization figure at the end of this lecture
|
Focus on how NSAIDs work… like we are going to be doctors… and like should know this (at least)
|
|
Lamina V describe why loss of large fibers increase pain
|
Loss of large fibers normally are inhibitory (when non-noxious stimulus); therefore loss of this inhibitory input increases pain sensitivity
|
|
What is secondary hyperalgesia?
|
The SC via NMDA receptors becomes sensitized to specific pain stim; therefore “pre-emptive” analgesia is used to plastic changes do not happen in the spinal cord (even with general anesthesia)
|
|
Review amazing Lamina Diagram… draw and label if you want
|
|
|
What lesions cause thalamic pain?
|
Lesions in the medulla, mesencephalon, or thalamus→ essentially if the spinothalamic tract is disrupted along length
|
|
“Where” is pain in the cortex?
|
S1 and also in the cingulated… there are studies I can send if you are interested
|
|
What happens if you activate large fibers?
|
If you activate large fibers you can decrease pain; remember inhibitory activity… large and small fiber activity act as a gate for pain
|
|
|
→You produce analgesia; this is mediated by the projections from PAG medulla 5-HT (serotonin) cells of the nucleus raphe magnus to lamina I and V in dorsal horn (inhibit firing) →PAG cells have high [opiate receptors]; then opiates bind, and descend to inhibit the lamina I and V
|
|
Lecture 18: Clinical Demonstration: Movement disorders
|
|
|
What is a tremor
|
1. repetitive movement with frequency (regular); 2. Also has a specific location (hands fingers toes)
|
|
TRAP for PD what does it mean
|
T→ tremor; R→ rigidity; A→ Akinisia; P→ postural abnormality
|
|
What is the characteristic PD posture & walk
|
Flexed arm, flexed knee; tiny steps/ little to no arm swing; during Romberg test the patient will often fall back
|
|
What is TX for PD?
|
1. L-Dopa (side effects include dyskinesia [extra uncontrolled movements]); 2. Dopamine agonists- don’t get dyskinesias (short term) (side effects include drowsiness, sudden sleep onset); 3. DBS- this inhibits overactive area of STN, can modulate, but invasive
|
|
What is an action tremor?
|
Small physiological tremor in everyone, modulated by hunger, caffeine, sleep etc.
|
|
Essential tremor
|
Type of familial benign tremor, alcohol is the best tx to get rid of the tremor
|
|
HD characteristics
|
Chorea (dance) irregular non tremor-like movements
|
|
Dystonias
|
Think cervical dystonia- can use Botox to inhibit muscles, thought to be mediated via BG abnormality
|
|
Orofacial dyskinesia
|
Abnormal involuntary lip and tongue movements (choreaform)
|
|
Signs of CB damage
|
1. intention tremor (tremor during conscious movement); 2. Loss of coordinated automatic movemtns (ataxia); 3. Unable to learn new motor skills (but depends on side of CB damage)
|
|
Which CB peduncle is input only?
|
The middle CB peduncle; the superior is mostly output, with some input; the inferior has both input and output
|
|
Describe CB information flow
|
1. afferent fibers enter; 2. 2 projections [one to the cortex & one to the deep nucleus]; 3. Cortical activation; 4. Output neurons (purkinje cells) project to deep nuclei; 5. Deep nuclei fibers project out of CB
|
|
What are the main inputs to the CB?
|
1. vestibular nucleus (CN 8); 2. Spinal cord (sensory); 3. Pontine nuclei; 4. Reticular formation; 5. Inferior olive
|
|
Where to vestibular afferents enter?
|
Vestibular afferents project to the flocconodular lobe and the vermis, they enter through the inferior peduncle
|
|
Where do the spino CB tracts enter and info?
|
SpinoCB tracts enter though the inferior peduncle; there are 4 that project to anterior and posterior CB in gross somatotopic fashion;
|
|
How many maps in the CB?
|
There are two maps [ one in the anterior CB lobe, the other in the posterior] that are not highly organized [oriented head to head around the primary fissure]
|
|
Where do cortical afferents go in CB?
|
CorticopontoCB tract go to pontine nuclei, cross, and enter the contralateral CB hemisphere [form most of the mossy fibers];
|
|
What does reticuloCB tract do?
|
Carries corollary discharges associated with postural adjustments of axial muscles and head & eyes
|
|
OlivoCB tract
|
Largest single source of fibers into CB; redundant path [carries sensory and motor info]; they end as climbing fibers
|
|
Lesion of olives causes?
|
The same as if you have lesions to the CB
|
|
Major CB outputs
|
1. from deep nuclei (dentate example) efferent exit sup CB ped; innervate contralateral VL thal, then projects to motor cortex
|
|
Where do fibers from interposed and fastigial go?
|
They primarily exit the sup CB ped, but travel to the red nucleus; cells from red nucleus project in the rubrospinal tract
|
|
What is Gait Ataxia?
|
Wide irregular unsteady “dunken sailor’s”
|
|
What are other CB [damage] signs?
|
Hypotonia- lack of tone against passive movement; Lack of check- inability to stop actions quickly; tremor- intention tremor [worst at end of movement]; dysarthria; Nystagmus
|
|
Titubation
|
Is a truncal tremor
|
|
Molecular layer made of?
|
Mostly fibers but occasional stellate and basket cells
|
|
Characteristics of Purkinje cells
|
1. only source of output (to deep nuclei); 2. Dendritic tree is flat and fan shaped; 3. Perpendiclular to the folia
|
|
Characteristics of Granule cells
|
1. most numerous cell in brain; 2. Send fibers to the molecular layer, they run parallel to the folia, and interact with multiple purkinje cells; 3. Small cell body
|
|
Characteristics of basket cells
|
1. located deep in the molecular layer; 2. Similar to purkinje cells but smaller and dendritic tree is less dense; 3.
|
|
Stellate cells
|
Smaller than baskets; highly branched synapse on purkinje cells
|
|
Diagram mossy fiber inputs to CB
|
1. Dorsal spino CB tract enters via inferior CB ped; 2. ventral spino CB tract via sup CB ped; bring sensory and propioceptive info; 3. Reticulo spinal CB tract from head through sup; 4. CCT from arms via inferior
|
|
Vesibular inputs from
|
The vestibular nucleus via inferior CB ped
|
|
Cortical inputs
|
CortocopontoCB via middle CB ped
|
|
Postural control input
|
Reticular input from reticular nucleus, via inf CB ped; to the vermis and flocconodular lobe
|
|
Error system origin?
|
Climbing fibers from the inferior olive to all parts of CB
|
|
Diagram the outputs of the CB
|
Dentate→ VL/VA thal; interpositus→superior ped to red nucleus; fastigial→ reticular and vest nuclei
|
|
|
|
|
|
|
|
|
|
|
Main cortex cell type
|
Pyramidal cells
|
|
Describe cortical layers output & input
|
|
|
Synergists are?
|
In this instance: muscles that contribute to the same action
|
|
Characteristics of slow twitch?
|
1. long term-contraction; 2. Small twitch tension; 3. Little fatigueability; 4. Oxidative only; 5. Motor neuron tonic discharg
|
|
Characteristics of fast twitch?
|
1. high intensity short duration; 2. Large twitch tension; 3. Rapidly fatigue; 4. Anaerobic metabolism; 5. Motor neuron phasic discharge
|
|
What are the 3 kinds of motor neurons?
|
1. alpha- innervate fast & slow muscles; 2. Gamma- innervate contractile portion of spindle; 3. Beta- innervate all three
|
|
What do the two types of interneurons do in SC?
|
1. coordinates motor output between synergistic (& inhibits antagonist); 2. Provides feedback inhibition to motor neurons to regulate output
|
|
What is the final common pathway?
|
The alpha motor neuron, when it fires the cells it connects to (motor unit) will contract
|
|
Where do the cell bodies lie (alpha)
|
In the ventral horn of the SC, how is it layed out? Most ventral is extensiors (more dorsal is flexors) distal motor is lateral
|
|
What are the afferent types and characteristics
|
I (Ia Ib)- 13-20 micrometers (80-120 meters/sec)
|
|
Intrafusal vs. extrafu-sal characteristics?
|
Intra- they are the muscle spindles
|
|
Info about intrafusal fibers
|
1. ends still contract; 2. Middle contains bag (dynamic stretch sensors) and chain fibers (more receptive to absolute length)
|
|
Describe monosynaptic reflex arc
|
1. stretch excites the Ia afferent; 2. Signal to SC excites Ia efferent to stim same muscle, inhibit antagonist; 3. Central control causes contraction of gamma to keep sensor taught
|
|
What does spinal circuitry do?
|
1. Generates rhythmic patters of movement; 2. Muscle tone; 3. Coordinate reflexes; 4. Compensates for fatigue
|
|
Where are flexors, extensors, proximal/distal represented in ventral horn of SC?
|
Extensors are most ventral, flexors dorsal, proximal is medial and distal (like fingers) is lateral
|
|
Order that motor units activated?
|
Smallest recruited first, then larger, etc, this done because the smallest are the most finely controlled and smooth force progression
|
|
Reciprocal inhib is?
|
The concurrent stim of synergistic muscle and inhibition of antagonist muscles; this is mediated by the interneuron pool
|
|
Myotatic reflex does?
|
Automatic load compensation during movements and postures; unexpected changes in load increase/decrease muscle force
|
|
Clasp-Knife does
|
Mediated by golgi, there to stop damage (from too much activity from happening)
|
|
What is the flexion/extension reflex?
|
When you step on a nail the ipsilateral foot is flexed (withdrawn) and the contralateral leg is extended; therefore you stay upright
|
|
Spinal shock is?
|
Loss of reflexes following cord transection; reflexes return within months and it is thought to be mediated through the loss of normal signal to the SC cells→hyper-reflexia
|
|
(Again) what innervates extra and intra muscles
|
Extrafusal muscles- force are innervated by the alphas
|
|
Please give origin and termination of
|
|
|
Lat-vest-spinal tract
|
O: lateral and vestibular nuclei; T: Ipsilateral cord all levels
|
|
Med-vest-spin-tract
|
O: medial and descending vest nuclei; T: bilateral cervical cord innervating neck muscles
|
|
Reticulo-spinal tract
|
O: medullary and pontine reticular formation T: all levels of contralateral cord
|
|
Rubro-spina l
|
O: red nucleus; T: contralateral cord (mainly cervical in humans)
|
|
Cortico-spinal
|
O: cortex Brodmann’s areas (BA) 4,6,3,1,2,7 ; T: conralateral cord all levels
|
|
Bilateral lesions of cortico-spinal cause?
|
Initially quite deficit (type of spinal shock?); then recovered most function; couldn’t ever control fingers
|
|
Bi- lesion rubro = ?
|
This leads to slightly more proximal difficulties
|
|
Rubro + cortico-spinal tracts are?
|
This is the lateral system and is responsible for fine, and distal limb movements
|
|
Vestibulo-spinal lesions cause?
|
Could not sit up (medial system) but could do all of the lateral movement things (e.g. fine finger and arm movements)
|
|
Which system does the vermis use?
|
The midline via fastigial nucleus to medial systems (reticulospinal & vestibulospinal)
|
|
What then do paravermis and hemispheres use?
|
To the lateral descending system
|
|
Where do the fibers come from in corticospinal system
|
55% from BA 4, 35% from BA 3,2,1, and 10% from association cortex
|
|
What are some targets of the cortico-spinal tract
|
Brainstem (both motor and sensory structures); red nuc, reticular formation, inferior olive, lateral redic, gracilis nuc, cuneatus nucleus; biggest one is interneurons in SC
|
|
What are some functions of inter-neurons?
|
coordination: 1. agonist/antagonist at a single joint via reciprocal innervation; 2. Complex multiple limb movements flexion withdrawal reflex; 3. Rhythmic movements
|
|
Differences between the lateral and medial descending pathways
|
Origin; lateral are only crossed, medial are bilateral; lateral usually contact MN directly medial doesn’t
|
|
What layer does the cortico-spinal tract arise in?
|
Layer 5 Betz cells (gigantic)
|
|
What is encoded in M1 (BA 4)
|
Force, “groups of muscles”, direction of movement, sensory signals related to movement, context that a muscle is used
|
|
What are the general points of vest system
|
Wholly subconscious; 2. Multimodal (equilibrium vision inputs); 3. Adaptable (constantly changing growth) landsickness
|
|
2 main parts of vest?
|
Otolith organs (utricle & saccule) which detect head tilt and linear accelerations & semicircular canals which detect rotations
|
|
Sensory epithelium of otoliths is?
|
Macula; hair cells imbedded in membrane which also has otoliths imbedded; head tilt induces it to pull on the cilia
|
|
Where is the saccule
|
Just beneath the utricle, perpendicular to saccula (macula orientation)
|
|
What is the sensory epi set up on the semicircular cannals?
|
Ampula is the region of dilatation, there is a stiff region the cupula that moves in the ampulla. Endolymph rotation induces movement opposite that of head roation
|
|
Where is the vest. Ganglion, what does it connect?
|
Scarpa’s ganglion in the internal aud. Meatus, has bipolar ganglion cells that innervate the hair cells and form part of 8th nerve
|
|
What are the parts of the vestibular gangia?
|
1. superior; 2. Medial; 3. Lateral; inferior → each of these has a specific set of connections with the 3rd, 4th, 6th nuclei for VOR
|
|
Lateral vest nucl input is from?
|
(Deiter’s nucleus); receives input from the macula of the utricle; sends output to the vestibulo-spinal tract mostly for the antigravity muscles
|
|
Medial and sup get input from?
|
Mostly cristae of the semi-circular cannals; axons send input to MLF [which mediate eye and neck movements]
|
|
Inferior get input from?
|
(descending vest-nucl) gets input from both semi-circ and maculi of utricle and saccule;
|
|
Vestibular reflexes divisions?
|
1. vision- attempts to stabalize image on retina [eyes shift opposite direction of head-DOLLS EYES [dead]; 2. Postural- ; 3. Righting- brings head to horizontal irrespective of the body position- head righting is lost if otoliths are destroyed
|
|
What mediates postural reflexes
|
Lateral vestibulospinal tract, mainly to gamma motor neurons which change muscle done (alpha a fair amount too); TONIC drive also gives tone to muscle
|
|
What is the vestibulocollic reflex
|
Just like VOR but for head (think chicken walk)
|
|
What does the VOR do to muscles?
|
Head turn L, Eyes rotate right; therefore you must stimulate the muscles on the R and inhibit the ones on the left; this is done by contralateral input (R semi inhibits L side muscles)
|
|
What are the functions of the Outer, middle, inner ear?
|
Outer (pinna and aud canal)- amplify and filter sounds; Middle (cavity and ossicles- amplify pressure and alow gain control; inner- cochlea
|
|
How does the pinna amplify sound? Aud cannal?
|
It collects sounds over a wide area and projects it towards the auditory canal; Auditory canal acts as a resonant chamber for sounds in the range of voice; this is up to 20 dB (100x)
|
|
Why does the middle ear exits (or at least one reason)
|
The middle ear exists so that you can collect pressure on the tympanic membrane and transduse it to fluid (which requires 20 time more force) without middle ear you loose 30dB
|
|
How is gain controlled in the middle ear
|
The tensor tympani muscles (analogous in fxn to pupil) which are innervated by (CN V)—maleus and incus; stapedius from facial nerve CN VII
|
|
What is the helicotrema
|
End of the basilar membrane space; connection between the scala vestibuli and scala typani
|
|
Describe the spatial frequency on basilar mem
|
Stiff at start floppy at end, related to where basilar is most deformed with differing frequencies
|
|
Organ of Corti is?
|
The name given to the sensory/motor/membranes that make sound transduction possible
|
|
Why is sound transduced by the hair cells
|
Because hair cells are deformed due to being imbedded in two types of membranes with different properties of stiff/floppy; motion opens ion channels
|
|
Why don’t you get single ear deficits?
|
There is lots of cross-talk between the ears throughout the auditory system. Therefore you don’t get deficits (lasting)
|
|
What are the three main auditory paths?
|
1. Classical- this is the most important for understanding; 2 & 3. Are interested in determining the source location of sounds
|
|
Classical pathway
|
1. spiral ganglion; 2. Cochlear nucleus→ acoustic stria and trapezoid body; 3. Inferior colliculus; 4. MGN; 5. BA 41
|
|
What are the parts of cochlear nucleus
|
The DCN → inferior colliculus (classical pathway)
|
|
What are the divisions of the inf colliculus?
|
1. central → largest component and is for the classical pathway [very sharp frequency tuning] also from LSO & MSO; 2. Pericentral → inputs from cortex and AVCN; 3. External → integrates somatosensory and acoustic inputs
|
|
Three subnuclei of MGN
|
1. dorsal→ broad tuning for frequency (no tonotopy [location?]); 2. Ventral→ primary for the classical pathway; 3. Medial → broad tuning but has tonotopic organization
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|
What does cortical (auditory) damage do in a human?
|
It decreases ability to localize and move towards (although you can reflexively respond) and you have difficulties with the specific timing and tone parameters (why speech is a problem)
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What does the MSO do?
|
It compares time of arrival in each ear do determine location of sound origin (for each frequency)
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|
Why does the LSO input from the contra ear stop off?
|
It needs to be changed to an inhibitory signal, by doing this you get to compare the absolute intensity that each ear received
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|
What is the trade off for rods vs cones
|
Rods are fast (and more sensitive to light) but slow to respond to following changes; cones can respond quickly but need more light to function
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|
What does light do to RM potential in cell?
|
It decreases the resting membrane potential (hyperpolarizing the cells)
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|
What is the threshold of independent sound discrimination?
|
About 1800 Hz in humans
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|
Which component of sound requires binaurality for effective discrimination?
|
Perception of the direction of propagation to localize sounds
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|
What are the components of the outer ear?
|
External meatus (auditory canal)
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|
Describe pinna function.
|
Amplification and directional filtering (ear most sensitive to sounds from the front)
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|
Describe external auditory meatus function.
|
Filtering through resonance. Especially good at amplifying frequencies between 2-6000Hz
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|
What kind of gain does the external ear provide?
|
About 20 db
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|
What implications does a less versatile, smaller pinna have for human hearing?
|
Amplification not as dependent on the pinna, localization not deterred
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|
What comprises the middle ear? What is its function?
|
Tympanic membrane
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|
How do the ossicles provide amplification?
|
Area ratio (tm: oval window, 20:1)
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|
How does the middle ear provide gain control?
|
Action of two muscles attached to the ossicles:
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|
Explain auditory hypersensitivity in Bell’s palsy and/or myasthenia gravis.
|
Loss of control over middle ear muscles prevent the ossicles from effectively dampening sound—can result in inner ear damage.
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|
What comprises the inner ear?
|
Cochlea (ventral)
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|
Where is the sensory apparatus of the ear located?
|
In the membranous labyrinth, tube contained within bony cochlea
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|
What is the modiolus?
|
Axis of the bony spiral
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|
Describe the relationship of the labyrinths within the cochlea.
|
Membranous labyrinth divides the osseous labyrinth into the scala vestibuli and the scala tympany
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|
What parts of the membranous labyrinth partition the scala vestibuli and scala tympani from the cochlear duct?
|
Reisner’s membrane and basilar membrane, respectively
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|
What is the cochlear duct?
|
Canal formed by membranous labyrinth
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|
Describe the path of sound from stapes to hair cell.
|
Stapes vibrates oval window. Pressure waves travel through scala vestibuli across the basilar membrane, dissipated by movements of round window. Meets hair cells in the organ of Corti on top of the basilar membrane
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|
Where is high frequency energy best transmitted along the basilar membrane? Why?
|
Through the basal end, near the cochlea, because it is stiffer there. Lower frequency waves may transmit through more of the basilar membane, and are generally “detected” at the apical end. This has to do with the variable compliancy of the basilar membrane: it is stiffer on the basal side near the cochlea and wider and more compliant at the apical end.
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Where is the round window? The oval window? How does the function differ?
|
The round window is at the end of the cochlea, at the end of the scala tympany. It helps dissipate the pressure waves.
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Describe changes in the displacement waves as they move down the basilar membrane.
|
The traveling wave increases in amplitude as it moves through the cochlea, until it reaches a point where it induces the maximal membrane movement. Then it dies out rapidly. The location along the membrane is characteristic for a particular frequency.
|
|
Described how sound frequencies are “mapped” along the length of the basilar membrane.
|
The changing characteristics of the basilar membrane make it differentially responsive to fluid pressure waves of varying frequencies. Because the membrane becomes more compliant and wider towards the apical surface (distal to the cochlear entrance), lower frequencies cause the greatest membrane displacement at points further along the basilar membrane than those of higher frequency.
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|
What is the organ of Corti?
|
Specialized epithelial structure on top oof the basilar membrane that contains the hair cells.
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|
What is the tectorial membrane?
|
Gelatinous “membrane” in which the stereocillia (microvilli) of the hair cells invests in. Movements of the basilar and tectorial membranes provides a mechanism for the detection of sound by transducing the pressure waves into electrical energy.
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|
How do hair cells transduce fluid pressure energy?
|
Bending hairs opens stretch-sensitive cation channels causing depolarization. Bending in the other direction causes hyperpolarization.. Depolarization causes transmitter release onto an auditory neuron, increasing the firing rate of neuron.
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|
Describe the path of sound transduction by the ear.
|
Sound→ tympanic membrane vibration→ ossicle vibration→ oval window→ basilar membrane traveling wave→ shear of hair cell stereocilia→ cation flux→ receptor potential→ increase in transmitter release→ excitation of ongoing discharges in auditory neuron
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|
What are the types of hair cells? What do they do? Where are they located?
|
Inner hair cells located in row closest to modiolus. Sensory structures, communicate with brain via auditory neurons in nerve.
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|
How are inner hair cells innervated?
|
By radial fibers from bipolar cells in spiral ganglion. 20 radial neurons to 1 inner hair cells.
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|
How are outer hair cells innervated?
|
From olivocochlear bundle from contralateral superior olivary complex, mostly all direct efferent connections.
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|
What is characteristic frequency?
|
Frequency at which a particular hair cell is responsive (tip of V)
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|
How do characteristic frequencies of hair cells change along the basilar membrane?
|
High to low
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|
Describe the idea of “labeled lines”
|
Concept that types of stimuli are transmitted by particular cells. Particular hair cells transduce and transmit information about only a particular (sometimes group of) frequency (cies).
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|
What is “phase-locking” and what component of sound does it encode?
|
Encodes “timing” of acoustic events.
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|
How is sound intensity encodes?
|
Firing rate of individual neurons or by the number of activated fibers.
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|
How does the frequency range that a particular hair cell responds to, change with increasing amplitude?
|
The range becomes larger
|
|
How does the rate of firing change at the beginning and at the end of an auditory event?
|
Dramatic increase in firing at the beginning, drop off (below basal activity) when it ends.
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|
What is tonotopy?
|
Systematic arrangement of neurons according to their frequency tuning
|
|
Why is there such extensive bilateral convergence in the auditory system?
|
Sound localization
|
|
Describe “step 1” in the auditory system, from cochlea to brain stem.
|
Bipolar neurons (cell bodies in spiral ganglion) relay signal from hair cells in cochlea, through auditory nerve, intl brain stem.
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|
Describe the course of auditory nerve fibers from the brain stem cochlear nucleus to the inferior colliculus.
|
Fibers from cochlear nucleus decussate in the acoustic stria and trapezoid body
|
|
Where does the lateral lemniscus send collaterals as it ascends to the inferior colliculus?
|
Superior olivary complex
|
|
In what tracts do fibers from the cochlear nucleus cross the brainstem?
|
Acoustic stria
|
|
From where does the inferior colliculus receive projections? What is its function?
|
Lateral lemniscus (from cochlear)
|
|
To where does the inferior colliculus project?
|
Contralateral inferior colliculus
|
|
Where does the medial geniculate nucleus project?
|
To auditory cortex
|
|
What is are the auditory radiations?
|
Projections from MGN to auditory cortex
|
|
What are the components of the cochlear nucleus? How are the fibers organized?
|
Dorsal (DCN)
|
|
What different cell types are contained within the three tonotopic subdivisions of the cochlear nucleus?
|
DCN—fusiform, “pausers”
|
|
How do pausers, primary-like, and onset neurons function?
|
Pausers, respond with few spikes at onset of auditory stimulation, pause, then train of spikes for duration of stimulus
|
|
Secondary cells of the auditory processing system are contained within which structure? Give three examples.
|
Cochlear nucleus:
|
|
Where does the DCN project?
|
Pauser cells project to contralateral inferior colliculus
|
|
Where do onset cells project? From which region of the cochlear nucleus?
|
Onset cells project to pontine nuclei (then to inferior colliculi)
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|
Where do AVCN cells project? What type of cells are these?
|
Primary like cells project to the pontine nuclei
|
|
What are the direct and indirect pathways in acoustic processing? Which nuclei and cell types are involved?
|
Direct. From DCN to contralateral inferior colliculus. Pauser cells.
|
|
What function does the direct pathway have and how is this different from the indirect pathway?
|
The direct pathway is likely involved in sound identification while the indirect pathway integrates binaural information and contributes to sound localization
|
|
What are two binaural cues?
|
Interaural intensity differences
|
|
What is IID and what is the threshold for human detection?
|
Interaural intensity differences. Idea that contralateral ear detects a lower intensity sound.
|
|
What is ITD, what is the human threshold? How does this compare with the duration of an action potential?
|
Interaural time differences.
|
|
Which structure seems to be primarily responsible for binaural stimuli integration? Which nuclei contribute?
|
Pontine nuclei
|
|
What is the initial site for IID detection? What inputs does it receive?
|
Lateral superior olive
|
|
What is the NTB? Where does it project? What information does it receive? What kind of output does it have?
|
Nuclei of the trapezoid body
|
|
How does the LSO encode IID information?
|
Particular neurons have different selectivity for various IID, received from the AVCN and the NTB
|
|
Where is binaural time comparison occur?
|
Medial superior olive
|
|
Describes the composition of the MSO.
|
Ribbon of spindle-shaped cells with two primary dendrites (medial and lateral)
|
|
Where do inputs from the ipsilateral AVCN go (in the MSO)?
|
To the lateral dendrites.
|
|
Medial dendrites of MSO neurons receive information from ___?
|
Contralateral AVCN
|
|
How is the inferior colliculus divided?
|
Central
|
|
Where does the classical ascending pathway project?
|
Central nucleus of the inferior colliculus
|
|
What projects to the pericentral, external, and central nucleus of the inferior colliculus?
|
Pericentral—strong descending projection from auditory cortex
|
|
What region integrates SS and acoustic inputs?
|
External nucleus of the inferior colliculus
|
|
Which nucleus contains neurons with a well defined CF and sharp frequency tuning?
|
Central nucleus
|
|
How are frequencies represented in the central nucleus of the inferior colliculus?
|
Tonotopically (low dorsal, high ventral)
|
|
What nuclei comprise the MGN? Which is involved in the “classical” pathway?
|
Dorsal
|
|
From where do the other regions receive information?
|
Dorsal—pericentral nucleus
|
|
Which MGN nuclei are tonotopically organized?
|
Ventral and Medial
|
|
What BA is the primary auditory cortex? What are its inputs/outputs?
|
Area 41
|
|
Describe the different dimension of organization in the primary auditory cortex.
|
Tonotopic bands (medial high frequency→)
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|
Where are other auditory fields located? What is their function?
|
Belt around AI
|
|
What are the connections of AII?
|
Reciprocal with Dorsal MGN and project to pericentral nucleus of inferior colliculus
|
|
Describes the classical pathway.
|
Central nucleus of inferior colliculus→ ventral of medial geniculate→A1 of auditory cortex
|
|
Alternative pathway.
|
Pericentral nucleus of inferior colliculus->dorsal MGN→AII of auditory
|
|
What defects does a cortical lesion have on auditory function?
|
Sound localization and recognition of temporal sound patterns
|
|
Medial geniculate
|
CN: DCN, AVCN, PVCN
|
|
Be able to draw pathways
|
|
|
What type of image do the cornea and lens produce on the retina?
|
Real, inverted image
|
|
What types of photoreceptors does the human eye contain (two types and then subtypes)?
|
Rods
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|
What is the fovea? What photoreceptors are located here?
|
Central portion of the visual field
|
|
What properties of the photoreceptors allows for such high visual acuity in the fovea?
|
Cones are thinner, allowing for denser packing, and smaller area: cone ratio
|
|
What accounts for the “pit-like” appearance of the fovea?
|
Other cells between the light source and the photoreceptors are pushed aside to reduce light scattering
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|
Where are rods located? How might this affect how one looks at dim light and why?
|
Mostly in periphery
|
|
What are the three segments of a photoreceptor? What are the basic contents/function of each segment?
|
Outer segment: visual pigment molecules, responsible for absorbing light and generating the electrical signal
|
|
How does the structure of the photosensitive membranes in rods and cones differ?
|
Rods. Series of intracellular discs, surrounded by a separate outer envelope.
|
|
What are pigment epithelial cells? What is their function?
|
Epithelial cells on back of eye, in contact with photoreceptors
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|
Where are melanin granules located? What do they do?
|
Located in pigment epithelial cells
|
|
Describe turnover of the outer segments.
|
Discs are continuously made and shed from the tip of the outer segment.
|
|
Describe the structure of visual pigments in rods and cones.
|
Similar structure in both. Protein portion and a chromophore, 11 cis-isomer of vitamin A (retinal)
|
|
What is the general structure of the rod pigment?
|
Rhodopsin contains opsin (7 transmembrane protein) and chromophore (retinal) that lies between the helices of opsin
|
|
Why does rhodopsin appear to be red? How does this property correspond with the ability to see dim light?
|
Absorbs light near 500 nm, which is bluish-green
|
|
What happens when retinal (bound to the protein) absorbs light?
|
11-cis→ all-trans form producing metarhodopsin II. Involves activation of G-protein cascade, all-trans retinal released from opsin by hydrolysis
|
|
What are the light reactions in the phototransduction cascade?
|
Photoisomerization of retinal from 11-cis to all-trans
|
|
What are dark reactions?
|
The reactions following photoisomerization of 11-cis retinal that proceed spontaneously
|
|
What does it mean that light “bleaches” rhodopsin?
|
Light causes photoisomerization of retinal to all-trans form which is eventually cleaved from the opsin molecule.
|
|
How does the photoreceptor “unbleach”?
|
11-cis is regenerated enzymatically and spontaneously rejoins opsin
|
|
What proteins are involved in the light-activated signal transduction pathway? What do they do?
|
Metarhodopsin II (all-trans retinal-opsin) stimulates transducin (GTP-binding protein)→ activates cGMP phosophdiesterase→ hydrolysis of cGMP→ closes cGMP-gated cationic channels
|
|
What is the end result of cGMP hydrolysis?
|
Closing of cGMP-gated cationic channels
|
|
What happens when metarhodopsin II binds transducin?
|
Exchange of GDP for GTP, resulting in activation of cGMP PDE
|
|
Describe the deactivation of the phototransduction pathway.
|
Metarhodopsin II is phosophorylated by rhodopsin kinase and binding of arrestin
|
|
Alpha-subunit of transducin?
|
|
|
What is “bradyopsia”? What can cause it?
|
Slow vision, diminished visual acuity for moving objects
|
|
What is the polarization state of the outer segment in darkness? In lightness? What causes this?
|
Dark: depolarized, cationic channels open
|
|
How is stimulus strength encoded by photoreceptors?
|
Response amplitude
|
|
What is the threshold of stimulation that will result in photoreceptor hyperpolarization? What is required for conscious perception of light?
|
1 photon
|
|
What is thermal isomerization of rhodopsin and how does this relate to dim light perception and the stability of rhodopsin?
|
Thermal isomerization is the decay of rhodopsin. Since it is indistinguishable from light-mediated bleaching, sets a limit on ability to perceive dim light
|
|
How do the synapses of photoreceptors onto horizontal and bipolar cells differ from regular synapses?
|
Ribbon synapses, contain 100s of vesicles and release increases steadily as function of membrane production
|
|
What is the NT released by photoreceptors and how does light affect this release?
|
Glutamate
|
|
What types of glutamate receptors are involved in the post synaptic response and how does this define bipolar cell types?
|
Metabotropic→ depolarization→ “On” cells
|
|
How do on and off cells respond to light?
|
On cells (metabotropic) depolarize in light
|
|
What are other names for on and off bipolar cells?
|
D and H bipolar cells
|
|
How is the retina organized?
|
Photoreceptors and horizontals to bipolars and horizontals in outer plexiform layer
|
|
What are amacrine cells? Where are they located and what are inputs/outputs?
|
Diverse group of neurons forming the inner plexiform layer
|
|
What is the “direct path” in the retina?
|
Photoreceptor→ bipolar→ RGC
|
|
What are the different types of bipolar cells, other than “on” or “off”?
|
Rod bipolars (receive input from multiple rods)
|
|
Similarly, what are the different types of RGCs?
|
Midget ganglion cells (usu 1 midget bipolar)
|
|
How does the spatial resolution of parasol cells related to that of midget cells?
|
Lower spatial resolution
|
|
Which NTs are released by the retina (and by which cells)?
|
Glutamate: rods, cones, bipolars
|
|
What are interplexiform cells?
|
Neurons that relay info from inner layers of retina back to horizontal cells in outer plexiform layer
|
|
How does a horizontal cell respond to light? What type of stimulus is best to activate this response?
|
Graded hyperpolarization
|
|
What is a receptive field?
|
Region of retina that influences the activity of a cell when stimulated by light
|
|
What is a receptive field “surround”?
|
Region around center of receptive field that gives opposite response to light (than center)
|
|
Why would a light falling on both the center and surround of a receptive field elicit any bipolar cell response?
|
B/c surround signals are delayed by traveling through additional synapse
|
|
What type of stimulus that most depolarized the Off-bipolar?
|
Dark spot on bright background
|
|
How do negative feedback synapses regulate surround of receptive fields in bipolars? What cell types is responsive to this?
|
Horizontal cells modulate response of photoreceptors presynaptically.
|
|
Why do bipolar cells have center surround receptive fields?
|
Important form of data compression that gives more significance to points of contrast rather than intensity at every point
|
|
What is spatial contrast?
|
Degree to which a region is brighter or darker than surrounding regions
|
|
Most ganglion cells carry which type of information?
|
Most have center-surround receptive fields, so carry information about spatial contrast
|
|
How is surround receptive field mediated for retinal ganglion cells?
|
Response of bipolar cells (on-bipolar cells antagonized by light in surround)
|
|
What are two major classes of ganglion cells?
|
Magnocellular (parasol), respond transiently and have larger receptive fields, spatial and temportal contrast
|
|
What is univariance? How does this apply to color processing?
|
Any receptor with a single binding site cannot encode identity of ligand (wavelength) separately from concentration of ligand (intensity)
|
|
What is an action spectra?
|
Measurements based on light responses
|
|
Describe structure of the three cone pigments.
|
Similar to rhodopsin. 7-tm protein, with chromatophore
|
|
What is protanopia?
|
Red-pigment lacking color blindness
|
|
What is deuteranopia?
|
Green-pigment deficient color blindness
|
|
What is tritanopia?
|
Blue-cone lacking color blindness
|
|
Which is the most rare?
|
Tritanopia
|
|
What is anomalous trichromacy?
|
Trichromatic but have a mutation which shifts the absorption spectrum of one of the pigments
|
|
What is achromatopsia? What causes this?
|
Failure to see colors but not patterns, with normal cones
|
|
How might one view the color red given non-white illumination?
|
Computation of “reflectance” from ratio of reflect and incident spectral intensities
|
|
What are double color opponent cells? Where are they located?
|
Located in parvocellular layer of LGN
|
|
Chapter 27: Visual System I
|
|
|
What are scotomas?
|
Regions of blindness in the visual field
|
|
What is diplopia when does it happen?
|
It is double vision; it occurs for multiple reasons the most important being the fact that CN or CN nuclei are damaged
|
|
What parts of each eye does the R monocular hit
|
R monocular hits L temporal and R nasal
|
|
Describe path of visual information starting at fovea (to cortex exclude brainstem stopoffs)
|
1. hit fovea- travel to optic nerve; 2. Leave eye as optic nerve; 3. Both nasal portions cross at the chiasm; 4. LGN; 5. Optic radiations [ upper bank in parietal is lower visual field], Meyer’s loop (lower bank) is in temporal lobe; 6. Cuneate- lower visual field & Lingual- upper visual field
|
|
Describe other light pathways
|
1. Suprachiasmatic nucleus- SCN above the chiasm, gets info about light/day conditions, helps entrain circadian rhythm sends output to pineal; 2. 10% of info goes to BS (two places) a. to the superior colliculus, b. to the pretectal nucleus→E-W nucleus→ciliary ganglion→ constrict muscles
|
|
What optic N. called after chiasm?
|
Optic tract- it not has information from only one hemi-field
|
|
Right optic tract cut deficit
|
Both eye L visual hemi-field= L homonymous hemianopsia
|
|
Thalamo-cortical path is responsible for (cognitive)
|
The things we normally associate with vision, perception, object recognition, depth perception, color vision
|
|
stimulate sup colic in monkey what happens
|
You evoke saccadic eye movements, important as it is subconscious, brings eyes to interesting things (e.g. flash)
|
|
What is E-W input, output and action
|
Input is from the pretectal nucleus which somehow calculates light intensity; output Is parasympathetic to the ciliary ganglion→ iris sphincter muscles to constrict
|
|
Which layers are contralateral in LGN; who cares?
|
1/4/6; I remember 1+4 = 5 is contra
|
|
One possible function of LGN?
|
To ensure that visual information from each eye is precisely aligned before being sent to the cortex
|
|
Which layers ore P & M
|
1 & 2 are M; 3→ 6 are P and carry color information and center surround info
|
|
What are the M cells good at then?
|
They are very good at timing issues, where as P are not→ nor is the downstream cortical area
|
|
What is the koniocellular pathway
|
This is a new (ish) path that carries blue info to the cortex; it is between the other LGN layers
|
|
Why synapes at LGN if no info transformed?
|
It receives input from cortex and probably acts as a gate; (from fact that only 10% of synapses are LGN, rest cortex)
|
|
History note→
|
Much of the primary visual cortex was mapped during WWI due to the high number of people with damage from bullets (I just like this fact… a lot… just takes an observant eye/brain)
|
|
How is info transformed at cortical level
|
Info goes from spots (on/off center) to line segments; ~80% of cells in V1 are orientation selective; these cells also display direction (movement) selectivity
|
|
What are the exceptions to orientation select
|
Some V1 cells have receptive fields that are the same as LGN (on off center cells)→ maybe important for timing?
|
|
What are the two main cells types in V1?
|
Stellate and pyramidal cells; most stellate are in layer IV, most pyramidal are in 2,3,5,6
|
|
What are the response prop in other than layer 4
|
They are complex in general, and send their output to other cortical areas
|
|
How is orientation selectivity organized
|
Orientation colums (cortical layers 1-6) all respond best to the same line orientation
|
|
As you travel across cortex how does orientation select change?
|
1 & 2 columns; 3 shows that orientation selectivity smoothly changes from column to column (can hit 90 degree switches though)
|
|
How quick does the change occur (distance)
|
About 10 degree change every 25-50μm (180 degrees/ 0.5-1 mm)
|
|
Hubel and Wiesel thought it was a grid, but how is it really?
|
Not layed out in a grid, more complex, but the idea is the same
|
|
What are CO blobs what do they do?
|
CO blobs are the regions that get color information in V1 and are insensitive to orientation
|
|
What does each square mm of cortex contain
|
All the machinery necessary to analyze one patch of visual field for orientation, color, and eye of origin→ together this is a functional module or hypercolum
|
|
Where are the binocular cells?
|
They are in layer 3 and get input from layer 4 from both eyes; but those closest to the border for each eye are the most binocular
|
|
In general what does the striate cortex do?
|
1. efficiently represents important features (lines etc); 2. Unifies both eye input; 3. Functional architechture for line orientation
|
|
What is extrastriate visual cortex?
|
Cortex outside of V1 that deals with vision, but is processing higher level (more complex/abstract) representations
|
|
What are the 2 main visual pathways
|
1. dorsal pathway→ concerned with where things are (“where” pathway, might be better to think about as “how” path… how would I act on a ball for example): 2. Ventral pathway→ “what” pathway responsible for determining the specific object (what it is, not caring about where)
|
|
What is blindsight
|
Ability of people (without conscious perception) to act correctly on visual stim, mediated by sup colic
|
|
What does visual agnosia mean
|
“agnosia” not knowing
|
|
Apperceptive agnosia
|
These people cannot copy; can’t recognize due to more visual deficits
|
|
Associative agnosia
|
These people can copy, but have problems with the semantic or visual object recognition point; they may be able to recognize when presented physically etc.
|
|
What is extinction
|
Can “see” in both R and L visual fields but if stimulated in both at the same time, misses one of the stimuli (always on the contralateral side to damge)
|
|
What is ventral simultagnosia?
|
Patients have difficulty perceiving multiple objects (no matter where they are in space)
|
|
Cerebral akinotopsia
|
These patients have difficulty sensing motion, and is often from damage that includes the posterior middle temp gyrus (like MT)
|
|
Cerebral achromatopsia
|
Inability to precieve color (usually damage is unilateral, as is the deficit)→ associated damage: inferior occipitotemporal cortex BA 37/19
|
|
Prosopagnosia
|
Iniability to recognize faces, in this deficit you selectively loose the ability to distinguish familiar objects (faces, birds (if a birder), goats, etc.)
|
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Monkey studies and lesion location object vs. landmark
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Monkey MT does
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Motion; receives input from the direction selective cells; think cerebral akinotopsia
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V4
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Color area (think cerebral achromatopsia); fine discrimination; major output is to temporal areas “what” path
|
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Attention influence general principals
|
Many areas of higher/association cortex don’t respond to visual stimulation without the modulation of either being awake or attentive (or both); essentially you can block out processing and access to consciousness if you focusing
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What (again) are the input layers of cotex
|
4c alpha & 4 c beta
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Neglect in humans
|
“Oh I missed something on that page? It must be on my left I guess.”
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Define sleep
|
1. little movement; 2. Stereotypic posture; 3. Reduced response to ext. stim; 4. And it is reversible
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|
What are the EEG properties of wake
|
Low voltage fast (16-25 Hz) ossilation
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|
Sleep stages and EEG findings
|
Stage 1: EEG decreases, EOG slow rolling eye movements, theta waves 3-7 Hz
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What is the sleep cycle and progression
|
|
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Sleep onset and consequences
|
Retrograde amnesia→ can’t remember a phone call or page in night, sleep deprived can enter REM directly,
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How does sleep change as we age
|
At birth 16-18 hours w/o consolidation → progression to consolidation and sleep ~8 hrs/day→ old age can’t sleep in later phase of sleep morning so up early (need naps)
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How is motor activity inhibited during REM
|
By the pontis oralis inhibitory connections to the ventromedial medullary reticular formation
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|
Important edocrine changes
|
1. Human growth hormone is stimulated by sleep (typical time, but increased greatly if you are asleep); 2. TSH peak in the late evening but are suppressed by sleep; 3. Melatonin from the pineal is secreted during sleep, function is unknown; 4. Prolactin increased greatly in sleep (both sexes); 5. Gonadatropins, (LH) and FSH: first released during sleep in puberty, LH secreted during sleep and not wake
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What does the pontine locus coeruleus do? Who else does this
|
Stimulates wakefulness; also by 1. Midbrain dorsal raphe nuclei; 2. Tuberomamilary nucleus, basal forbrain, lateral dorsal tegmentum,
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How is NREM mediated
|
Active inhibition of most of the neurons in the hypothalamus, temp may mediate this
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|
How is REM mediated?
|
Cholinergic neurons in the basal forbrain, lateral dorsal tegmentum and pedunculopontine nuclei are active during REM
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|
What do high/low amplitude EEG signify
|
High amp signifies synchrony it has nothing to do with activity low equals asynchronous→ likely from thalamocortical oscillations
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|
Insomnia means
|
Difficulty initiating or consolidating sleep (20-33% of people have), shor sleep time, or non-restorative sleep
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|
Narcolepsy
|
Tetrad of symptoms: 1. Cataplexy [sudden loss of muscle tone]; 2. Excessive daytime sleepiness; 3. Hypnagogic hallucination (dream-like experiences at sleep onset); 4. Sleep paralysis (conscious but unable to move)
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|
Apnea 2 kinds
|
1.
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|
2.
|
central → CHF and premature/ young infants possibly because BStem isn’t mature
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Parasomnias
|
Movements and behaviours occurring during sleep; sleepwalking, night terrors, RLS
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|
Facts about sleepwalking
|
First third of night; 15 seconds →30 min; sitting, standing, walking, fumbling with objects
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|
RLS
|
Strong almost compulsive desire to move legs, often feelings of things crawling in lefs, worse if the leg is at rest; treated with dopamine drugs
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|
Night terrors
|
Stage 3 & 4 sleep most common in children; terrified and scream; sleep terrors are usually not remembered
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|
REM sleep behavior disorder
|
Man fights wolf from eating wife→ really hitting wife
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|
Physiologic changes in sleep
|
1. active heat loss; lower volume more concentrated urine; less digestion; decreased responsivity to senses
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|
What does sleep do to TSh levels
|
It actively suppresses TSH thereby decreasing metabolism
|
|
What are the 3 main stages of dev?
|
1. neuron generation (neurogenesis); 2. Extend axons (pathway/target selection); 3. Selecting the correct connections (address selection)
|
|
Where is the zone of proliferation?
|
Near the ventricles→ cells here divide and eventually give rise to the whole nervous system
|
|
Interkinetic nucl migration
|
The progression from G1 → mitosis and the location that each timepoint the cell portray (diagramed above)
|
|
What is the order of cell generation
|
From the inside out (later neuons must migrate through previous layers to get to their specific spot)
|
|
How is position related to generation time?
|
The early time points end up in earlier layers (6 & 5) that the ones that divide later “birthdating”
|
|
What does a radial glia do?
|
Provides a guide to the migrating neuron
|
|
Why design a system where the cell has to move?
|
In this way the cell can sense the environmental signals and determine what type of cell to become
|
|
When are neurons and glia made
|
In general neurons are made first, once this is complete the glia are made, tumors may arise from these remaining NSC in the SVZ
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|
What happens to the radial glia after dev
|
The radial glia actually degenerate
|
|
How do cells (in layers) know what to become?
|
Determined by environment, but early cells (layer 6) multipotent (later cells like 3) cannot go back to being layer 6 cells only forward to 1,2 etc.
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|
How do NSC know to make glia
|
Neurons make glial growth factor with inhibits NSC from making neurons, then they make glia
|
|
How are axons guided?
|
axons have growth cones →
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|
What are guidpost cells
|
Just what they sound like, they are waypoints that the cell has to pass in order to reach its destination
|
|
What is required for early circuitry development?
|
Molecular cues, but the later fine circuitry development is based upon activity
|
|
What is the visual critical period?
|
The idea that correct vision (no strabismus cataracts etc) is required to accurately prune and finalize the circuit
|
|
What happens if you cover an eye during critical period?
|
If an eye is covered during the critical period it is devoid of stimulation; the adjacent area (in this case other eye) gobbles up the cortex [uses it itself]
|
|
What does the above test tell you?
|
That stimulation is required for normal wiring; that if quiet, adjacent areas make stronger connections and use the “unused” cortex
|
|
So what mechanism explains this phenomenon
|
Competition; this is a constant act; through practice or experience we get better [one reason] because cortical areas gobble up more to have more cortical representation
|
|
How could you prove activity is required?
|
Inject TTX into cat’s eyes [bilateral]; no ocular dominance formed, b/c there was no competition→ this is the exact experiment that was performed to prove this
|
|
At the cellular level how could competition change wiring?
|
Wiring could be changed by LTP/LTD mechanisms to the point that if a synapse isn’t used (or some low threshold) the synapse is endocytosed [while more & stronger connections of the others are made]
|
|
Why does this competition lead to lasting structural changes?
|
The cells during the critical period are competing for limited resources (neurotrophic factors); when they don’t get enough they retract
|
|
What can this competition allow?
|
It can allow the matching of the number of pre & post synaptic terminals
|
|
Glia make up __% of brain cells
|
90% of cells, but because they are smaller about 50% of volume
|
|
What are the two main classes of glia
|
1. microglia→ are phagocytes that mobilize after injury, infection or disease [derived from meso not ecto]; 2. Macroglia→ the main type of glia in the brain→ two main tys the astocytes and oligodendrocytes
|
|
What is know about the fxn of astrocytes
|
Both have end-foot dilations that contact and surround the capillaries and arterioles throughout the brain (BBB); they also envelope synapses
|
|
What are the two types of astrocytes
|
Protoplasmic & Fibrous→ they may have different functions but it isn’t know, they are probably different cells (from different lineage) as their surface has different proteins expressed
|
|
What are the two types of oligos?
|
1.
|
|
2.
|
interfasicular- white matter
|
|
What do perineuronals do
|
Adhere to somas of neurons (not myelinating)… the might actually be microglia and not astrocytes (unknown)
|
|
And interfasicular
|
Myelinate axons from 1-30 of them
|
|
What are the main proteins in myelin
|
1. proteolypid protein (PLP)-- transmembrain; 2. Myelin basic protein (MBP)—cytoplasmic
|
|
Where/when do glia develop
|
They develop in the SVZ following neurons; they also migrate along the radial glia
|
|
What controls oligo dev? And why is the number perfect for myelination?
|
It seems as though neurons control the # of oligos, there are no bare patches and no spare oligos; PDGF (platelet-derived GF) increases oligo division (made if astrocytes are close to electrically active neurons)
|
|
What happens to the others?
|
They undergo apoptosis (about 2x as many are mad as are needed)
|
|
What is distinct about glia membrane properties vs neurons
|
No dendrites; axon; or synapes; -90 mV resting membrane potential; therefore primarily permeable to K+
|
|
Why can K+ be taken up by glia? What is it called?
|
K+ can be taken up b/c of nernst equation; therefore the glia “buffer” by quickly taking up K+
|
|
What do astrocytes do?
|
Unknown (but lots of theories); structural support; insulate synapes; maintain ECF [K+]; BBB; nourish neuons; promote neuronal survival (via trophic factors); synapse formation; NT spillover (re-uptake)
|
|
What happens to neurons w/o glia?
|
You can form synapes (but low #) and they are 100 times less active
|
|
What are the different types of memory?
|
Declarative (explicit/episodic/recent) memory
|
|
What is declarative memory?
|
Memory that mediates conscious recollection of events and facts
|
|
How can declarative memory be tested?
|
Presentation of words/items to remember, and after a delay ask to recognize or recall items
|
|
What type of memory is impaired in global amnesia? What is global amnesia?
|
Declarative memory
|
|
What sort of lesion characterizes anterograde amnesia?
|
Medial-temporal brain regions (HM) or
|
|
What sort of lesion did HM have?
|
Bilateral medio-temporal lobectomies
|
|
What is Korsakoff’s syndrome?
|
Consequence of long-term alcoholism (usually) or vitamin deficiency that leads to progressive destruction of the periaqueductal or periventricular regions that may spread to the mamillary bodies
|
|
How might unilateral medio-temporal lobe or diencephalic damage present?
|
As material-specific amnesia (left-sides with learning verbal material, right-sided with learning nonverbal material)
|
|
What lesion might result in an inability to learn new verbal material?
|
Due to a left sided medial-temporal or diencephalic lesion
|
|
What evidence is there that medial temporal lobe structures are not involved in storage of long term memory?
|
HM did not have retrograde amnesia, must mean that those memories are stored elsewhere. However, MT lobe is important for consolidation of declarative memory
|
|
In what disease is there progressive damage to entorhinal and hippocampal brain regions? What type of memory does this impair?
|
Alzheimer’s disease
|
|
Developmental abnormalities are common to which two disorders?
|
Schizophrenia
|
|
What region may be important for emotional aspects of memory?
|
Amygdala
|
|
What is procedural memory?
|
Memory that mediates forms of skill learning
|
|
How is procedural memory measured?
|
By progressive improvements in speed or accuracy by a subject across different sessions
|
|
What is classical conditioning? To which type of memory is it most closely related?
|
Association learning between some unconditioned stimulus with an unconditioned response to form a conditioned response
|
|
What type of memory is frequently impaired in individuals with basal ganglia disease? What are three examples?
|
Usually skill learning (procedural memory)
|
|
What types of learning/memory are impaired with cerebellar disease?
|
Skill learning and classical conditioning (procedural memory)
|
|
What is repetition priming?
|
Change in speed, accuracy, or bias with which repeated stimuli are processed relative to either their initial processing or some baseline
|
|
Do most amnesiac patients have normal or abnormal repetition priming?
|
Normal
|
|
What is perceptual priming?
|
Form specific processes involved in stimulus identification
|
|
What is conceptual priming?
|
Meaning-related processes involved in stimulus comprehension
|
|
Plasticity in modality-specific input cortices (like visual, auditory, etc) is demonstrated with which kind of priming?
|
Perceptual priming
|
|
Which type of priming is associated with multi-modal (association) cortices?
|
Conceptual priming
|
|
Repetition priming is associated with more or less activation in cortical regions?
|
Less
|
|
What is working memory?
|
Mnemonic processes involved in temporary storage of information being presently used
|
|
What are “memory buffers”
|
Refer to areas of brain that hold information
|
|
What are executive working-memory processes?
|
Hold goal-oriented information in mind and guide mental and motor action
|
|
Where are the executive working-memory regions located?
|
Prefrontal neocortex
|
|
What type of memory processes are important for strategic memory performance?
|
Executive working memory
|
|
Why might HD or PD patients have trouble with executive working memory deficits?
|
Frontal lobes may be impaired or basal ganglion may play a role (b/c of communication with frontal lobe structures)
|
|
Is working memory the path to long term memory?
|
No. These are actually processed in parallel.
|
|
In the most general sense what is aphasia?
|
It is a disturbance in the ability to understand or produce speech (but not motor deficits) e.g. grammar/syntax
|
|
Can deaf (signers) get aphasia?
|
Yes; therefore this machinery isn’t simply for sound interpretation but for grammar and syntax
|
|
What is syntax
|
The grammatical structure of sentences
|
|
What are language issues based on motor problems called?
|
Dystarthria→ this is important because dysarthria leaves language comprehension completely intact
|
|
How is the language circuit conceptualized now
|
A series of regions that perform functions on the material and form bidirectional communication (neural network)
|
|
What does a broca’s aphasic sound like
|
Telegraphic speech, correct nouns, slow, halting, usually unable to repeat sentence unless highly stereotyped (but meaning is there); called nonfluent; also can’t determine who does the action in reversible sentences “the boy was kicked by the girl” who kicked who?
|
|
Wernicke’s aphasia
|
Speech is fluent (in that it is effortless sounding), but utterly meaningless; they make lots of paraphasias
|
|
What is a paraphasia? Who cares
|
When you select the wrong word for your meaning, there are semantic- ocean vs pond apple vs lemon
|
|
Global aphasia
|
Usually from and M1 occlusion of the MCA (whole L hemisphere) person can’t really comprehend or produce
|
|
What is sham rage?
|
Characteristic set of behaviors elicited by removal of the neocortex and dorsal part of diencephalons (in cats)
|
|
Stimulation of the VM hypothalamus may lead to what types of behaviors (in cats)?
|
Defensive behaviors
|
|
Stimulation of the L hypothalamus may lead to what types of behaviors (again, cats)?
|
Attack behaviors
|
|
Describe the Papez circuit
|
Major connection between hypothalamus to cortex: through mamillary bodies to anterior thalamus to cingulate gyrus
|
|
What are the major components of the limbic system?
|
-amygdala
|
|
What is Kluver-Bucy syndrome?
|
Results from bilateral temporal lobe ablations
|
|
What does Kluver-Bucy indicate for the role of limbic structures?
|
Lots of things: in particular that may be involved in selective attention (esp amygdala)
|
|
Lesions of which area produce an increase in sham rage/aggression?
|
Septal nuclei
|
|
Where are benzodiazepines most effective at inducing their anxiolytic effects?
|
In the amygdala
|
|
What is the primary site of action of cocaine and amphetamines?
|
At the nucleus accumbens (DA-ergic inputs from VTA)
|
|
What are the primary drug actions of cocaine and amphetamine
|
Cocaine: block reuptake of DA
|
|
What is the primary site of action of opiates?
|
VTA
|
|
Review the paths to and from the amygdala and hippocampus.
|
|
|
Where is the amygdala located?
|
Deep to the medial surface of the temporal lobe
|
|
What are the different amygdalar nuclei?
|
Corticomedial group (cortical, medial, central nuclei)
|
|
What are the afferents to the central nucleus?
|
From other limbic structures: septal nuclei, VMH
|
|
What are the afferents to the basolateral amygdala?
|
Limbic: cingulated cortex, DM and intralaminar thalamus
|
|
What are the two major efferent amygdalar tracts?
|
Stria terminalis: VM and medial preoptic hypothalamus)
|
|
What are other connections from the amygdala?
|
Direct projection to prefrontal cortex
|
|
What comprises the hippocampal formation?
|
Hippocampus, dentate gyrus, subiculum, entorhinal cortex
|
|
Describe the cortical composition of the hippocampal formation
|
Allocortex. Hippocampus and dentate have archicortex (three layered) while entorhinal is six layered. The subiculum shows the transition from 3→6 layers
|
|
What is ammon’s horn?
|
Hippocampus proper
|
|
Describe the internal connections of the hippocampal formation.
|
Most inputs to formation go to entorhinal
|
|
What are the perforant pathways?
|
Projections from entorhinal cortex to the granule cells in the dentate gyrus
|
|
What type of fibers project from the granule cells of the dentate gyrus to Ammon’s horn? What cell type do they terminate on?
|
Mossy fibers
|
|
What are the most prominent cell type of the dentate gyrus?
|
Granule cells
|
|
What does CA refer to?
|
Cornu ammonis
|
|
What are CA-4 and CA-3 projections called? Where do they go to?
|
Schaeffer collaterals
|
|
Where do cells of the hippocampal commissure originate?
|
Dentate gyrus and ammon’s horn
|
|
What is the psalterium?
|
Fiber tract of hippocampal commissure
|
|
How do inputs to entorhinal cortex compare with inputs to the amygdala?
|
Entorhinal inputs are from the association cortices and represent polymodal sensory areas
|
|
Where do the efferents from the subiculum go?
|
To the fornix (anterior thalamus, mamillary bodies, cingulated cortex)
|
|
What extrinsic connections project to areas of the formation outside of the entorhinal cortex and subiculum?
|
Locus coeruleus and Raphe nucleus to ammon’s horn
|
|
What are the components of the septal region?
|
Lateral and medial septal nuclei
|
|
Name the major septal nuclei efferents
|
Amygdale and hippocampal formation and anterior and DM thalamus
|
|
What are the major afferents of the septum?
|
Input from reticular system: raphe, locus coeruleus, substantia nigra
|
|
Which hypothalamic area sends diffuse projections all over the neocortex?
|
Lateral hypothalamus
|
|
Lecture 36: fMRI
|
|
|
What is the basis for BOLD
|
Detection of oxygenated vs deoxygenated blood, this changes the field strength and therefore the MR signal; you can detect on a second time scale and it is analogous to the specific regions requiring blood
|
|
What does increased signal mean in fMRI?
|
It means the area is engaged in processing, but has no information as to whether or not it is required for a specific function
|
|
DTI
|
Measures white matter tracts (diffusion tensor imaging) looks at restricted (spatially) diffusion of H2O
|
|
Diffusion clinical reason
|
Clinically this is the most important scan for stroke. It is sensitive within minutes to the decoupling of metabolism and restricted diffusion
|
|
What does the anatomy of the corpus callosum (CC) tell you about function
|
The CC anatomically connects areas of the brain in very stereotyped ways: anterior does anterior structures of the brain, posterior the same (e.g. striate, temporal, parietal)
|
|
What is “a” main function for the CC
|
Inerhemispheric transfer of information
|
|
How does one communicate with the R hem
|
Use as little verbal information as possible
|
|
What is the R hem good at?
|
Spatial manipulation and other nonverbal skills
|