Neuro Flash Cards

Front 1

Properties of AP?

Back 1

1. big/fast; 2. All or none; 3. Invariant; 4. Conducted rapidly; 5. Refractory period

Front 2

Ion direction with NA+/K+ pump?

Back 2

2 Na+ is pumped out, 3 K+ is pumped in

Front 3

EPSP definition?

Back 3

Excitatory post synaptic potential—the depolarization that the dendritic spine undergoes (passive spread/depolarization)

Front 4

What is responsible for all or none AP?

Back 4

The presence of voltage gated Na+ channels at the axon hillock

Front 5

Draw a simple reflex and describe mediators

Back 5

1. muscle spindle senses increased tension; 2. Afferent info travels to SC; 3. Synapses and feeds back to muscle of interest to increase tension

Front 6

Define divergence

Back 6

A sensory neuron may get info from multiple spindles (multiple specialized sensory regions), but feed to one neuron

Front 7

Define convergence

Back 7

Multiple sensory fibers impacting a single motor neuron

Front 8

What does the resting memb. potential represent

Back 8

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

Front 9

AP characteristics?

Back 9

~1 ms; 0.1 volt amplitude; overshoot (because Na+ closed and K+ open [cell goes to K+ equilibrium]; all or none

Front 10

How are duration and intensity of stretch encoded?

Back 10

Duration of stretch= duration of AP “train”

Front 11

Draw the relationship (time and intensity) as described above

Front 12

What causes the relative refractory period? How long?

Back 12

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

Front 13

What mediates absolute ref period?

Back 13

Mediated by “ball” [ball and chain model] that blocks the channel; this makes sure AP’s don’t travel in both directions

Front 14

Draw and exp. temporal summation

Back 14

Temp. sum. is a result of the lack of IMMEDIATE voltage dissipation within the cell dotted line = threshold

Front 15

Exp. spatial summation

Back 15

Cell gets multiple input from axons at same time, these sum at the axon hillock, but come from spatially distinct dendrites

Front 16

IPSP

Back 16

Inhbitory post synaptic potential; usually used Cl- to “buffer” a cell from reaching threshold

Front 17

Properties of local potentials

Back 17

1. graded [not AP]; 2. Travel passively; 3. Dissipate quickly

Front 18

What does Nernst eq. do?

Back 18

Describes the voltage across the membrane in terms of K+

Front 19

What is happening with ions in equilibri

Back 19

There is no net movement of charge

Front 20

What are general bits of info re: [ions] in/out & voltage.. don’t memorize

Back 20

Ion Out In Eq. Pot.

Front 21

Most cells selectively perm to what?

Back 21

K+; they have a straight curve for [K+] vs. rest mem potential

Front 22

What determines the rest mem potential?

Back 22

The ion concentrations and the charges on each side of the membrane = electrochemical equilibrium

Front 23

Does the [ion] change much?

Back 23

NO; it is mostly charge that moves when the membrane depolarizes not a significant number of ions

Front 24

How much (%) can Na/K ATPase use?

Back 24

Incredible amounts 60-80% of some neurons needs, this now makes sense that even resting the brain uses 20% of O2

Front 25

Draw the difference in membrane potential vs. [K+] for both glia and neurons; why does this happen (in general)

Back 25

the cell is also permeable to Na+

Front 26

What is the Goldman equation; how is it different from Nernst

Back 26

Goldman takes into account multiple ions, Nernst is generally set up only to take into consideration K+

Front 27

Why is an EPSP depolarizing?

Back 27

The action of neurotransmitter opens Na+ channels which move down both electrical and chem. gradient into cell

Front 28

What are the 4 main characteristics of AP?

Back 28

1. all or none; 2. Threshold for AP generation; 3. Refractory period; 4. The AP doesn’t dissipate with increasing distance

Front 29

Why is there an AP threshold at all? What range is considered to be threshold?

Back 29

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

Front 30

This is one of the most important things you will learn… Why does the AP initially decrease?

Back 30

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

Front 31

What are the slower K+ channels called?

Back 31

Delayed-rectifying potassium channels (due to their 1 msec delay in opening in response to the voltage change)

Front 32

Which channel type primarily determines the AP of a cell?

Back 32

The K+ channels, because they are the ones responsible for repolarization; e.g. is the cardiac calcium-dependent Ca++ channel diagramed here

Front 33

What do TTX and STX block?

Back 33

TTX- Tetrodotoxin & STX- saxotoxin both block Na+ channels

Front 34

What are the toxins that block K+? Who cares?

Back 34

TEA- tetraethylammonium; 4-AP- 4- aminopyridine; these have been useful to determine membrane properties via examination of a single type of ion channel

Front 35

How do local anesthetics work? Antitiarrythmics?

Back 35

e.g. lidocaine works by blocking the Na+ channels, can also decrease cardiac excitability

Front 36

How does voltage normally spread down a conduit? Why need APs?

Back 36

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

Front 37

What is the length constant? Why care?

Back 37

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

Front 38

Why does the AP travel in only one direction?

Back 38

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

Front 39

What is the node spacing in myeliniated axons?

Back 39

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

Front 40

What is hyperkalemic periodic paralysis?

Back 40

“ball-and-chain” is damaged; therefore patient uses up all ATP then collapses to the floor

Front 41

What are the main kinds of neuronal connections?

Back 41

1.

Front 42

2.

Back 42

Minor- Electrical- fast, invariant response

Front 43

How is NT released?

Back 43

In “quanta” essentially vesicles – although new research shows that some areas have “kiss-and-run” therefore non-quantal release

Front 44

What is a MEPP?

Back 44

Miniature end plate potential; it is the depolarization from the release of one (or a few) vesicles of NT

Front 45

What are characteristics of Lambert-Eaton

Back 45

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)

Front 46

How to vesicles release contents? Who cares?

Back 46

V & T-snare hypothesis; Ca++ allows the binding, capture, and release of NT within vesicles.

Front 47

Why does Lambert-Eaton show a U shaped curve

Back 47

because there is a slow accumulation of Ca++ in the synaptic buton allowing more vesicles to release contents [this is called facilitation]

Front 48

What is the omega profile?

Back 48

It is the EM pic of a vesicle fused (very illustrative)

Front 49

What happens at buton for NT release?

Back 49

1. AP travels down axon; 2. Volt sense Ca++ channels open; 3. Vesicle fuses through V&T-snares; 4. NT released into cleft

Front 50

How is [Ca++] decreased in buton?

Back 50

Via possible mitochondrial buffering; Ca++ pumping out of buton

Front 51

What are the actual proteins in V&T snare hypothesis?

Back 51

V-Snares→ synaptobrevin

Front 52

What would increased [Ca++] do to vesicle release?

Back 52

The increased [Ca++] would tend to increase the vesicular release because it is required for snare binding

Front 53

Where are places where kiss and run happens

Back 53

The retina is a place where quantal release does not happen always (specifically the rods and cones)

Front 54

How does botox work?

Back 54

Botox is a zinc endopeptidase (there are multiple) that is targeted to some component of the NMJ (there are also multiple targets)

Front 55

What are some characteristics of NT?

Back 55

1. synthesized and concentrated in neurons; 2. Released from neurons; 3. Local application mimics synaptic release; 4. There are mechanisms for removal of protein

Front 56

Where is ACh mainly found?

Back 56

it is the main NT at the neuromuscular junction, it is also used in the basal forebrain

Front 57

What NT is inhibitory?

Back 57

The main inhibitor in the brain in GABA (amino acid)

Front 58

What NT are in the monoamine class? Function?

Back 58

dopamine; 2. Serotonin; 3. Norepi; 4. Epi; 5. Histamine→ these are all based off the tryptophan & tyrosine; -----Function→ modulation of other NT

Front 59

What do the peptide NT do?

Back 59

Conrol hypothalamic pituitary axis; feeding/sexual behavior

Front 60

Where are NT released?

Back 60

from the synaptic buton; in quanta (usually); in an active zone (can be seen on EM)

Front 61

How is NT loaded into cells?

Back 61

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

Front 62

What is the rate limiting step in Catecholamine syn? Who cares?

Back 62

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

Front 63

What are the Catecholamines?

Back 63

Tyrosine→ L-Dopa→ Dopamine→ Norepinephrine→ Epinephrine

Front 64

What are the fates for dopamine

Back 64

1. degradation by COMT/MAO; 2. Reuptake and degradation; 3. Reuptake and repackaging

Front 65

How is cocaine thought to work?

Back 65

Through the inhibition of dopamine transport (therefore there is increased dopamine in the cleft)

Front 66

How are Amphetamines thought to work?

Back 66

Crank, X (works same way); disrupt proton gradient allowing NT leakage (not through vesicle fusing)

Front 67

clinical ways to increase dopamine?

Back 67

L-Dopa (precursor); MAOi (monoamine oxidase inhibitor); COMT

Front 68

ACh degraded how?

Back 68

AChE; choline take into buton; combined with Aceyl CoA= ACh

Front 69

How do VX and Sarin gas work?

Back 69

They inactivate AChE, this causes too much ACh in the cleft and paralysis (because you run out of ATP)

Front 70

How is glutamate recycled?

Back 70

Glutamate uptake into glia; converted to glutamine; shuttled to neurons and made back into glutamate

Front 71

How are Neuropeptides made?

Back 71

They are proteins; therefore made in ER→ Golgi→ endosomes → released; because a protein must be resynthesized

Front 72

What are brisk reflexes indicative of?

Back 72

Upper motor neuron damage; long term this has increased tone; together this is termed spacticity

Front 73

What would getting knifed in the back give you?

Back 73

1. A very bad day; 2. Brown-Sequard syndrome: ispilesional weakness, loss of Big 4; contralateral loss of little 3

Front 74

Drawbacks & good of electrical synapses?

Back 74

1. no amplification is possible; 2. Cell sizes matter (usually cells are same size)… Good → fast; bi-directional

Front 75

2 main classes of a chemical synapse

Back 75

1. directly gated/coupled (receptor for NT and channel in same protein); 2. Indirectly gated/coupled→ GPCR (usually)

Front 76

Benefits of indirect coupling?

Back 76

1. allows for massive amplification; 2. Allows for changes in gene expression; 3. Allows multiple signals to converge

Front 77

What causes Myasthenia Gravis?

Back 77

Immune reaction against the AChReceptors (causing endocytosis)

Front 78

What are the two main drug classes for seizures? Function?

Back 78

1. Diazepams→ act as GABA agonists (increasing inhibition); 2. Valproate→ increases GABA synthesis

Front 79

Define direct coupling

Back 79

NT receptor and channel are part of the same complex

Front 80

Inhibitory synapses included which ions?

Back 80

Mainly Cl- and K+ because both tend to polarize cell (move cell further from threshold)

Front 81

Can inhibitory signals depolarize the cell?

Back 81

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

Front 82

What does Succinyl choline do? Why?

Back 82

Flaccid paralysis; this is because it keeps ACh like action in the cleft for a long time, this desensitizes the NMJ

Front 83

Best plasticity catch phrase?

Back 83

“Fire together wire together”

Front 84

How do we think memory is formed [generally]

Back 84

We think that long term potentiation & depression (LTP/D) forms the basis for the changes in weighting given to neurons

Front 85

What’s the difference between AMPA and NMDA receptors?

Back 85

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.

Front 86

What does Ca++ do?

Back 86

Ca++ activateds CaMKII (which can phosphorylate lots of stuff); KO mice lack LTP; loading a cell with CaMKII mimics LTP

Front 87

What is the end result of this stuff?

Back 87

More AMPA receptors are expressed at the surface; therefore higher depolarization with each incoming signal

Front 88

Differences between LTP/D?

Back 88

high frequency vs. low frequency stimulation

Front 89

Describe Hippocampus pathway

Back 89

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

Front 90

What are the main divisions of PNS

Back 90

1. sensory; 2. Motor; 3. Autonomic (which is divided into sympathetic and parasympathetic)

Front 91

Bundles of nerves are called?

Back 91

fasicles

Front 92

Draw the parts of the nerve bundles and label

Back 92

Epineurium- most outside tough—collagen and epithelial cells)

Front 93

How do PNS axons grow back? Speed?

Back 93

Through the sheath that remains used for guidance; grow back about 1 mm/day

Front 94

Where are sensory neuron cell bodies

Back 94

DRG

Front 95

Number and division of SC roots

Back 95

31 roots; 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal

Front 96

How are mechano-receptors specialized?

Back 96

They can be specialized to detect vibration, light touch, temp, chemicals, pain→ this is accomplished via the end organ

Front 97

What do propioceptors do?

Back 97

they bring fine motor information re: limb and muscle position

Front 98

What are muscle spindles? Do?

Back 98

specialized muscle cells (intrafusal) that wrap sensory axons; they contract and stretch to keep receptor sensitive;

Front 99

What are the two kinds of MS fibers? Info conveyed by?

Back 99

Nuclear chain- provide static info about length- IIa

Front 100

What are reflex arcs good for?

Back 100

1. coordinating movements; 2. (more importantly?) maintaining static position

Front 101

why …CNS damage cause hyperreflexia?

Back 101

The stretch reflexes are inhibitied via a connection from the CNS, if this inhibition is lifted the reflexes are enhanced

Front 102

channels that underly temp sense?

Back 102

TRP channels; have temp sensitive Na+ channels, these channels also respond to chemicals (e.g. capsacin)

Front 103

What are the two separate pain fibers?

Back 103

A delta- small myelinated carry fast info

Front 104

What is in a motor unit?

Back 104

1. motor neuron; 2. NMJ; 3. At least one muscle fiber (the units get smaller for fine control-e.g. eyes)

Front 105

Review muscle contraction

Front 106

Smooth muscle contraction

Back 106

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)

Front 107

ANS divisions and functions

Back 107

Symp- fight or flight- ACh then noreipi

Front 108

Which axon for both para/ sympathetic is the longer one? Who cares?

Back 108

→The sympathetic preganglionic axon is short (top)

Front 109

What does symp stim do to iris, salivary, sweat, bronchi, heart, GI, sex organs, bladder

Back 109

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

Front 110

How does caffeine work?

Back 110

antagonizes adenosine A1 receptor thereby increasing norepi release in the PNS and CNS

Front 111

What is the NT for para sympathetic?

Back 111

ACh only (pre & post ganglionic); remember ganglia are usually embedded in tissue

Front 112

Enteric NS (ENS)

Back 112

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

Front 113

What are some characteristics of Charcot-Marie-Tooth?

Back 113

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)

Front 114

Guillan Barre Syntrome

Back 114

GBS- rare autoimmune reaction (following URI or vaccination); sudden loss of both sensory and motor control; extensive supportive care is needed (as is immunosupression)

Front 115

Ulnar nerve palsy

Back 115

leaning on ulnar nerve (can been seen in alcoholics)

Front 116

what (specifically) provides a conduit for PNS regeneration?

Back 116

the perineurium, epineurium, and endoneurium; therefore surgical repair requires accurate aposition

Front 117

What myelinates PNS? Derived from?

Back 117

Schwann cells myelinate PNS; NCS derived, each Schwann myelinates only a single (portion) axon

Front 118

What is EMG and Nerve conduction used for?

Back 118

These measure speed of conduction, and also are a surrogate for the number of axons conveying information

Front 119

What covers the SC?

Back 119

The three layers of meninges; 1. Pia; 2. Arachnoid; 3. Dura

Front 120

# of spinal nerves from each segment?

Back 120

2 (remember bilateral)

Front 121

Gestalt of Big 4 path

Back 121

1. DRG gracile cunate fasiculi; 2. G & C nuclei; 3. Thal VPL

Front 122

Gestalt of little 3

Back 122

1. DRG neuron; 2. Synapse dorsal horn, cross in anterior white commisure; 3. VPL in thal to cortex

Front 123

Gestalt of CST (cortico-spinal)

Back 123

cortex, synapes with LMN in layer #9, out to muscle

Front 124

where does the SC end, where LP done?

Back 124

SC ends around L1/2; and LP is done @ L4/5 (in the lumbar cistern)

Front 125

draw each of the tracts and synapses, label neuron number

Front 126

DCML path neurons # and function

Back 126

1st cell body in DRG, synapses in G & C nuclei; 2nd G & C nuclei to the VPL thal; 3rd thalamus to the cortex

Front 127

Differences between spinothal & DCML?

Back 127

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

Front 128

annoying but important… layers and functions of SC areas… Draw

Front 129

What are Lamina I/ II?

Back 129

Marginal zone (I) Substantia gelatinosa (2) many spinothalamic 2nd order nerons have CB here

Front 130

What are Lamina III-VI doing?

Back 130

Nucleus proprius (forms the majority of the dorsal horn) processes sensory info (discussed later)

Front 131

Lamina VII

Back 131

Clarke’s nucleus between C8 –L2

Front 132

Lamina IX

Back 132

ventral horn motor neurons

Front 133

Lamina X

Back 133

periaqueductal grey- thought to do “something” with pain

Front 134

Again what is Brown-Sequard syndrome

Back 134

Hemisection of SC causing loss of Big 4 contralateral and little 3 ipsilateral; paralysis on side of section

Front 135

What are Betz cells? Where are they?

Back 135

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

Front 136

Signs of UMN damage

Back 136

hyper-reflexia and increased tone (from lack of inhibition)

Front 137

signs of LMN disease

Back 137

muscle wasting (chronic) hypo-reflexia, flaccid

Front 138

Draw and describe 4 main functional components of spinal nerves

Back 138

GSA- general somatic afferent- sensory BIG 4 & little 3

Front 139

Draw the circle of willis, describe what each vessel feeds

Front 140

occlude an ICA what happens?

Back 140

Generally nothing, that is why you have a circle of willis

Front 141

what is supplied by posterior circ?

Back 141

Brainstem, pons, occipital lobes (generally), and thalamus; infarction of the thalamus can mimic hemispheric MCA stroke

Front 142

Draw the circle again

Front 143

What are the most common branches for stroke

Back 143

The lenticulostriate areteries these feed the basal ganglia and the internal capsule

Front 144

Describe that path of the cartotid to M1 branch

Back 144

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

Front 145

Describe M1 MCA→ distal braches course

Back 145

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

Front 146

Describe the posterior circ branches and what they come off

Back 146

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

Front 147

Thing to remember when describing vasculature

Back 147

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

Front 148

What is unusual about brain veins?

Back 148

not usually with arteries, they don’t have valves

Front 149

Draw and label venous flow

Front 150

Basic concepts re: brain metabolism?

Back 150

Brain is hungy: 20% glucose, possibly 50% oxygen (resting requirements); <60 sec after blood flow stops unconscious

Front 151

How is cerebral blood flow maintained with changes in BP?

Back 151

Through autoregulation: therefore increases in BP don’t change tissue perfusion

Front 152

Describe they types of hemorrhages and causes

Back 152

Epidural- often from trauma, minndle meningeal aretery tears

Front 153

Draw and label ventricles (figure →)

Back 153

This is a great figure. Notice how anterior and posterior the horns traverse

Front 154

What is within the vents making CSF?

Back 154

Choroid plexus (yucky crappy looking stuff in dissection)

Front 155

Describe the flow of CSF

Back 155

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

Front 156

Cisterns of brain: what are they? What are a few? draw

Back 156

They are enlargements in the space for CSF

Front 157

Characteristics of normal CSF? function

Back 157

clear, colorless, odorless; functions to support brain (so it floats… 1400 gram brain weighs 50 grams while floating)

Front 158

Rate CSF made; amount of CSF in brain

Back 158

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

Front 159

Types of hydro

Back 159

1.

Front 160

2.

Back 160

non-communicating usually obstruction of aqueduct or other small communication

Front 161

Draw and label ventricles (figure →)

Back 161

This is a great figure. Notice how anterior and posterior the horns traverse

Front 162

What is within the vents making CSF?

Back 162

Choroid plexus (yucky crappy looking stuff in dissection)

Front 163

Describe the flow of CSF

Back 163

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

Front 164

Cisterns of brain: what are they? What are a few? draw

Back 164

They are enlargements in the space for CSF

Front 165

Characteristics of normal CSF? function

Back 165

clear, colorless, odorless; functions to support brain (so it floats… 1400 gram brain weighs 50 grams while floating)

Front 166

Rate CSF made; amount of CSF in brain

Back 166

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

Front 167

Types of hydro

Back 167

1.

Front 168

2.

Back 168

non-communicating usually obstruction of aqueduct or other small communication

Front 169

Big picture of BS

Back 169

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)

Front 170

What are two main reasons for unconsciousness? Differentiate?

Back 170

1.

Front 171

2.

Back 171

a lesion (possibly small) to the reticular formation

Front 172

What type of fibers arise from the Edinger westphal nuc

Back 172

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)

Front 173

What are the 5th nerve nuclei/function

Back 173

Mesencephalic- propioception; Principal sensory- light touch; spinotrigeminal- pain and crude touch

Front 174

First things to do when identifying BS nuclei

Back 174

Which part of the brainstem? Is it medial (efferent) vs dorsolateral (afferent)

Front 175

Why unilateral facial droop?

Back 175

This is due to the fact that UMN were damaged, UMN for the forehead is bilateral, but face is only unilateral

Front 176

What should you always do to make sure a patient is dead

Back 176

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)

Front 177

Nuclei in the pons?

Back 177

V-IIIV although 6-8 exit at the pontomedullary junction

Front 178

Which is the only nerve to exit dorsal

Back 178

The trochlear is the only nerve to exit dorsally, the trochlear also innervates the contralateral side

Front 179

What are & function of mixed nuclei

Back 179

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

Front 180

Pure sensory nuclei?

Back 180

1,2,8

Front 181

Pure motor nuclei

Back 181

3,4,6,11 (head/shoulder),12 (tongue movements)

Front 182

SSA & SVA

Back 182

SSA- hearing, vision, balance; SVA- olfaction & taste

Front 183

GSE

Back 183

Derived from mesoderm (tongue [12] and extraocular muscles [3,4,6])

Front 184

What are the rest of the muscles called?

Back 184

Branchiomeric as they develop from the brachial arches—they are innervated by the SVE

Front 185

SVE

Back 185

Motor of V, Motor of VII, Nucleus ambiguous (9,10) [controls striated muscles of larynx and pharynx], accessory 11

Front 186

GVE

Back 186

Parasympathetic preganglionic neurons, E-W (3), superior and inferior salivitory nucleus (7,9) [salivation and mucous glands], motor of vagus [10] heart lung gut

Front 187

Sensory include

Back 187

GVA/SVA; SSA; GSA

Front 188

GVA/SSA

Back 188

Solitary nucleus (7,9,10)→carotid body, larynx, pharynx, heart, lungs, guts

Front 189

SSA

Back 189

Choclear nucleus (8), Vestibular (8)

Front 190

GSA

Back 190

V1-V3 for trigeminal, mesencephalic nucleus of 5 (propiorception of jaw); principal sensory of 5; spinal trigeminal nucleus → pain and temp for head & neck

Front 191

Draw path of sense info to cortex from face

Back 191

Principal sensory of 5, VMP thal, to cortex; pain via spinal V nucleus

Front 192

Corticobulbar describes?

Back 192

It describes the motor tract for the face and neck (that rely on BS neuclei)

Back 193

VL-input BG (SNr GPi) CB; output to motor & premotor cortex

Front 194

Relay nuclei of the sensory system

Back 194

VPL- Body – DCML and spinothalamic output to sensory cortex

Front 195

The only sense that doesn’t go to thal?

Back 195

Olfaction goes directly to cortex

Front 196

What are the parts of diencephalon and their parts

Back 196

1. Epithalamus- pineal, habenular nuclei; 2. Subthalamus- STN functionally related to BG; 3. Hypothalamus- reg autonomic function and drive- behaviour

Front 197

What are the main thal projections?

Back 197

Diffuse projection nuclei, and relay nuclei

Front 198

General principles

Back 198

Connections with cortex are bi-directional; parallel info remains segregated in the thal e.g. pain light touch, joint postion in VPL

Front 199

What is the internal medulary lamina?

Back 199

It is a Y shaped band of white matter that divides the thal into three main sections: 1. Anterior; 2. Medial; 3. Lateral

Front 200

Draw and label thalamic nuclei, if you want state the connections

Front 201

VA & VL do?

Back 201

Input from BG, output to motor/premotor cortex

Front 202

VPM & VPL do?

Back 202

Inputs from sense BIG 4 & little 3; outputs primary sensory

Front 203

AV

Back 203

Limbic fuctions: input from hypothal via mamilothalamic, output to the cingulated (emotion & memory?)

Front 204

DM

Back 204

Limbic functions: input amygdala, olfactory cortx, output prefrontal cortex (planning, organizing behavior)

Front 205

Intralaminar nuclei

Back 205

Input – BS reticular activating system, spinal cord; output- frontal cortex, other Thal nuclei (regulates alertness, consciousness?)

Front 206

CM

Back 206

Most prominent intralaminar nucleus

Front 207

Reticular nucleus

Back 207

Input- corticothalamic and thamocortical collaterals

Front 208

What is thalamic pain syndrome?

Back 208

After damage even light touch can stimulate strong feelings of pain

Front 209

Pulvinar

Back 209

Projects, connects lots of parietal and temporal association cortex

Front 210

Lecture 15: Basal Ganglia

Front 211

What is the nucleus accumbens

Back 211

Anterior region where the head of the caudate and putamen join, part of reward center, think drug addiction

Front 212

Why do we consider caudate and putamen one structure

Back 212

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

Front 213

Striatum=

Back 213

Caudate + Putamen

Front 214

SNc vs SNr

Back 214

Pars compacta (SNc) vs Pars reticulata (SNr)

Front 215

What is the function of SNc?

Back 215

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

Front 216

What is hemibalism? Cause?

Back 216

It is uncontrolled movements of one side of the body; it is caused by STN damage

Front 217

Damage in PD?

Back 217

PD results from selective loss of neurons (dopamine containing) in the SNc → PD always think decreased movement (with rx)

Front 218

Board question: what does the BG do?

Back 218

“Gating of movements”

Front 219

Draw the BG circuit

Back 219

A circuit is diagramed below… use for reference

Front 220

Who are the players in the BG circuit?

Back 220

1. caudate; 2. Putamen; 3. GPe; 4. GPi; 5. STN; 6. SNr; 7. SNc

Front 221

BG principal input/output?

Back 221

Input- BG input from cortex to the caudate and putamen

Front 222

What (on movement) does activity in GPi/SNr do?

Back 222

Activity in these areas inhibits movement

Front 223

Where do direct / indirect path go?

Back 223

Direct- goes from caudate/putamen to GPi/SNr directly

Front 224

What does the direct path do in general?

Back 224

It inhibits the inhibitory output of BG; therefore it increases movement

Front 225

What are hyperkinetic movement diseases?

Back 225

HD- ultimately affects whole striatum, STN can’t be inhibited, so the inhibitory output (to stop movement) is inhibited so you get more movement

Front 226

Pacinian corpuscle does?

Back 226

Responds best to vibration & pressure

Front 227

Meissner?

Back 227

Responds to lower frequency vibration

Front 228

What kind of info to slow adapting and fast adapting carry?

Back 228

Slow adapting carry information (usually poor temporal resolution), but they tell you a stimulus is happening

Front 229

What do Golgi tendon organs tell you?

Back 229

They give you the tension that the muscle is under (they are hypothesized to stop (muscle) contracting if damage will occur

Front 230

Joint receptors tell you?

Back 230

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

Front 231

Anterolateral made of what?

Back 231

The spinothalamic & spinoreticulothalamic; pain/temp/crude touch

Front 232

How would you test the anterolateral sys?

Back 232

You could do hot/cold and pain (e.g. pin-prick)

Front 233

DC-ML?

Back 233

BIG 4 from body (except head)

Front 234

What is magnification re: brain tissue?

Back 234

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)

Front 235

How does the DCML sharpen information?

Back 235

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

Front 236

Describe two-point discrimination over body surface?

Back 236

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

Front 237

Where does sensory info project?

Back 237

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

Front 238

Map in 3a for?

Back 238

Most anterior for muscle afferents

Front 239

3b

Back 239

Slow and rapid adapting mechanoreceptors (aka fine touch)

Front 240

1

Back 240

Rapidly adapting neurons with slightly larger fields

Front 241

Most posterior (2)

Back 241

Receives input from joint afferents

Front 242

How does a doctor assess pain in pts?

Back 242

They really can’t; one must trust a patient… this is one reason that pain is such a huge problem

Front 243

Is pain a good thing?

Back 243

Acute paint is a warning (and useful); chronic pain is not

Front 244

Is pain objective? And features?

Back 244

No, it is not a stimulus→ “an experience”: components of pain actual stimulus, emotional, and cognitive

Front 245

What is allodynia?

Back 245

The perception of pain to normally non-painful stimuli

Front 246

hyperalgesia

Back 246

Increased sensitivity to pain

Front 247

How does aspirin reduce pain?

Front 248

What is the diff between nocioceptive and neuropathic pain

Back 248

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

Front 249

Why do C & A-delta respond to noxious?

Back 249

They generally have free nerve endings

Front 250

Why pain with nerve compression?

Back 250

The large fibers are the first to be KO and the nocioceptive small fibers are the last (remember cyanotic hand video)

Front 251

Without large fibers how is pain perceived

Back 251

All pain is perceived as burning in the absence of large fiber information

Front 252

How do NSAIDs reduce pain

Back 252

Inhibition of cyclooxygenase (which normally makes prostaglandins) and sensitizes nerve endings to pain

Front 253

Back to SC Lamina

Front 254

Lamina I; name? respond to?

Back 254

Lamina I; marginal zone; responds to noxious stimuli; many cell bodies in this lamina contribute to spinothal tract

Front 255

Lamina II; same drill as above

Back 255

Lamina II; substantia gelatinosa; small interneurons, many respond to noxious stim; primary afferent from small fibers

Front 256

Lamin III & IV

Back 256

Respond to BIG 4, does not increase activity to noxious stim

Front 257

Lamina V

Back 257

Inhibitory and excitatory effects to non- noxious stim; also excited by noxious stim

Front 258

Lamina VI

Back 258

Respond to joint movements

Front 259

Study the sensitization figure at the end of this lecture

Back 259

Focus on how NSAIDs work… like we are going to be doctors… and like should know this (at least)

Front 260

Lamina V describe why loss of large fibers increase pain

Back 260

Loss of large fibers normally are inhibitory (when non-noxious stimulus); therefore loss of this inhibitory input increases pain sensitivity

Front 261

What is secondary hyperalgesia?

Back 261

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)

Front 262

Review amazing Lamina Diagram… draw and label if you want

Front 263

What lesions cause thalamic pain?

Back 263

Lesions in the medulla, mesencephalon, or thalamus→ essentially if the spinothalamic tract is disrupted along length

Front 264

“Where” is pain in the cortex?

Back 264

S1 and also in the cingulated… there are studies I can send if you are interested

Front 265

What happens if you activate large fibers?

Back 265

If you activate large fibers you can decrease pain; remember inhibitory activity… large and small fiber activity act as a gate for pain

Back 266

→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

Front 267

Lecture 18: Clinical Demonstration: Movement disorders

Front 268

What is a tremor

Back 268

1. repetitive movement with frequency (regular); 2. Also has a specific location (hands fingers toes)

Front 269

TRAP for PD what does it mean

Back 269

T→ tremor; R→ rigidity; A→ Akinisia; P→ postural abnormality

Front 270

What is the characteristic PD posture & walk

Back 270

Flexed arm, flexed knee; tiny steps/ little to no arm swing; during Romberg test the patient will often fall back

Front 271

What is TX for PD?

Back 271

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

Front 272

What is an action tremor?

Back 272

Small physiological tremor in everyone, modulated by hunger, caffeine, sleep etc.

Front 273

Essential tremor

Back 273

Type of familial benign tremor, alcohol is the best tx to get rid of the tremor

Front 274

HD characteristics

Back 274

Chorea (dance) irregular non tremor-like movements

Front 275

Dystonias

Back 275

Think cervical dystonia- can use Botox to inhibit muscles, thought to be mediated via BG abnormality

Front 276

Orofacial dyskinesia

Back 276

Abnormal involuntary lip and tongue movements (choreaform)

Front 277

Signs of CB damage

Back 277

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)

Front 278

Which CB peduncle is input only?

Back 278

The middle CB peduncle; the superior is mostly output, with some input; the inferior has both input and output

Front 279

Describe CB information flow

Back 279

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

Front 280

What are the main inputs to the CB?

Back 280

1. vestibular nucleus (CN 8); 2. Spinal cord (sensory); 3. Pontine nuclei; 4. Reticular formation; 5. Inferior olive

Front 281

Where to vestibular afferents enter?

Back 281

Vestibular afferents project to the flocconodular lobe and the vermis, they enter through the inferior peduncle

Front 282

Where do the spino CB tracts enter and info?

Back 282

SpinoCB tracts enter though the inferior peduncle; there are 4 that project to anterior and posterior CB in gross somatotopic fashion;

Front 283

How many maps in the CB?

Back 283

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]

Front 284

Where do cortical afferents go in CB?

Back 284

CorticopontoCB tract go to pontine nuclei, cross, and enter the contralateral CB hemisphere [form most of the mossy fibers];

Front 285

What does reticuloCB tract do?

Back 285

Carries corollary discharges associated with postural adjustments of axial muscles and head & eyes

Front 286

OlivoCB tract

Back 286

Largest single source of fibers into CB; redundant path [carries sensory and motor info]; they end as climbing fibers

Front 287

Lesion of olives causes?

Back 287

The same as if you have lesions to the CB

Front 288

Major CB outputs

Back 288

1. from deep nuclei (dentate example) efferent exit sup CB ped; innervate contralateral VL thal, then projects to motor cortex

Front 289

Where do fibers from interposed and fastigial go?

Back 289

They primarily exit the sup CB ped, but travel to the red nucleus; cells from red nucleus project in the rubrospinal tract

Front 290

What is Gait Ataxia?

Back 290

Wide irregular unsteady “dunken sailor’s”

Front 291

What are other CB [damage] signs?

Back 291

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

Front 292

Titubation

Back 292

Is a truncal tremor

Front 293

Molecular layer made of?

Back 293

Mostly fibers but occasional stellate and basket cells

Front 294

Characteristics of Purkinje cells

Back 294

1. only source of output (to deep nuclei); 2. Dendritic tree is flat and fan shaped; 3. Perpendiclular to the folia

Front 295

Characteristics of Granule cells

Back 295

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

Front 296

Characteristics of basket cells

Back 296

1. located deep in the molecular layer; 2. Similar to purkinje cells but smaller and dendritic tree is less dense; 3.

Front 297

Stellate cells

Back 297

Smaller than baskets; highly branched synapse on purkinje cells

Front 298

Diagram mossy fiber inputs to CB

Back 298

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

Front 299

Vesibular inputs from

Back 299

The vestibular nucleus via inferior CB ped

Front 300

Cortical inputs

Back 300

CortocopontoCB via middle CB ped

Front 301

Postural control input

Back 301

Reticular input from reticular nucleus, via inf CB ped; to the vermis and flocconodular lobe

Front 302

Error system origin?

Back 302

Climbing fibers from the inferior olive to all parts of CB

Front 303

Diagram the outputs of the CB

Back 303

Dentate→ VL/VA thal; interpositus→superior ped to red nucleus; fastigial→ reticular and vest nuclei

Front 307

Main cortex cell type

Back 307

Pyramidal cells

Front 308

Describe cortical layers output & input

Front 309

Synergists are?

Back 309

In this instance: muscles that contribute to the same action

Front 310

Characteristics of slow twitch?

Back 310

1. long term-contraction; 2. Small twitch tension; 3. Little fatigueability; 4. Oxidative only; 5. Motor neuron tonic discharg

Front 311

Characteristics of fast twitch?

Back 311

1. high intensity short duration; 2. Large twitch tension; 3. Rapidly fatigue; 4. Anaerobic metabolism; 5. Motor neuron phasic discharge

Front 312

What are the 3 kinds of motor neurons?

Back 312

1. alpha- innervate fast & slow muscles; 2. Gamma- innervate contractile portion of spindle; 3. Beta- innervate all three

Front 313

What do the two types of interneurons do in SC?

Back 313

1. coordinates motor output between synergistic (& inhibits antagonist); 2. Provides feedback inhibition to motor neurons to regulate output

Front 314

What is the final common pathway?

Back 314

The alpha motor neuron, when it fires the cells it connects to (motor unit) will contract

Front 315

Where do the cell bodies lie (alpha)

Back 315

In the ventral horn of the SC, how is it layed out? Most ventral is extensiors (more dorsal is flexors) distal motor is lateral

Front 316

What are the afferent types and characteristics

Back 316

I (Ia Ib)- 13-20 micrometers (80-120 meters/sec)

Front 317

Intrafusal vs. extrafu-sal characteristics?

Back 317

Intra- they are the muscle spindles

Front 318

Info about intrafusal fibers

Back 318

1. ends still contract; 2. Middle contains bag (dynamic stretch sensors) and chain fibers (more receptive to absolute length)

Front 319

Describe monosynaptic reflex arc

Back 319

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

Front 320

What does spinal circuitry do?

Back 320

1. Generates rhythmic patters of movement; 2. Muscle tone; 3. Coordinate reflexes; 4. Compensates for fatigue

Front 321

Where are flexors, extensors, proximal/distal represented in ventral horn of SC?

Back 321

Extensors are most ventral, flexors dorsal, proximal is medial and distal (like fingers) is lateral

Front 322

Order that motor units activated?

Back 322

Smallest recruited first, then larger, etc, this done because the smallest are the most finely controlled and smooth force progression

Front 323

Reciprocal inhib is?

Back 323

The concurrent stim of synergistic muscle and inhibition of antagonist muscles; this is mediated by the interneuron pool

Front 324

Myotatic reflex does?

Back 324

Automatic load compensation during movements and postures; unexpected changes in load increase/decrease muscle force

Front 325

Clasp-Knife does

Back 325

Mediated by golgi, there to stop damage (from too much activity from happening)

Front 326

What is the flexion/extension reflex?

Back 326

When you step on a nail the ipsilateral foot is flexed (withdrawn) and the contralateral leg is extended; therefore you stay upright

Front 327

Spinal shock is?

Back 327

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

Front 328

(Again) what innervates extra and intra muscles

Back 328

Extrafusal muscles- force are innervated by the alphas

Front 329

Please give origin and termination of

Front 330

Lat-vest-spinal tract

Back 330

O: lateral and vestibular nuclei; T: Ipsilateral cord all levels

Front 331

Med-vest-spin-tract

Back 331

O: medial and descending vest nuclei; T: bilateral cervical cord innervating neck muscles

Front 332

Reticulo-spinal tract

Back 332

O: medullary and pontine reticular formation T: all levels of contralateral cord

Front 333

Rubro-spina l

Back 333

O: red nucleus; T: contralateral cord (mainly cervical in humans)

Front 334

Cortico-spinal

Back 334

O: cortex Brodmann’s areas (BA) 4,6,3,1,2,7 ; T: conralateral cord all levels

Front 335

Bilateral lesions of cortico-spinal cause?

Back 335

Initially quite deficit (type of spinal shock?); then recovered most function; couldn’t ever control fingers

Front 336

Bi- lesion rubro = ?

Back 336

This leads to slightly more proximal difficulties

Front 337

Rubro + cortico-spinal tracts are?

Back 337

This is the lateral system and is responsible for fine, and distal limb movements

Front 338

Vestibulo-spinal lesions cause?

Back 338

Could not sit up (medial system) but could do all of the lateral movement things (e.g. fine finger and arm movements)

Front 339

Which system does the vermis use?

Back 339

The midline via fastigial nucleus to medial systems (reticulospinal & vestibulospinal)

Front 340

What then do paravermis and hemispheres use?

Back 340

To the lateral descending system

Front 341

Where do the fibers come from in corticospinal system

Back 341

55% from BA 4, 35% from BA 3,2,1, and 10% from association cortex

Front 342

What are some targets of the cortico-spinal tract

Back 342

Brainstem (both motor and sensory structures); red nuc, reticular formation, inferior olive, lateral redic, gracilis nuc, cuneatus nucleus; biggest one is interneurons in SC

Front 343

What are some functions of inter-neurons?

Back 343

coordination: 1. agonist/antagonist at a single joint via reciprocal innervation; 2. Complex multiple limb movements flexion withdrawal reflex; 3. Rhythmic movements

Front 344

Differences between the lateral and medial descending pathways

Back 344

Origin; lateral are only crossed, medial are bilateral; lateral usually contact MN directly medial doesn’t

Front 345

What layer does the cortico-spinal tract arise in?

Back 345

Layer 5 Betz cells (gigantic)

Front 346

What is encoded in M1 (BA 4)

Back 346

Force, “groups of muscles”, direction of movement, sensory signals related to movement, context that a muscle is used

Front 347

What are the general points of vest system

Back 347

Wholly subconscious; 2. Multimodal (equilibrium vision inputs); 3. Adaptable (constantly changing growth) landsickness

Front 348

2 main parts of vest?

Back 348

Otolith organs (utricle & saccule) which detect head tilt and linear accelerations & semicircular canals which detect rotations

Front 349

Sensory epithelium of otoliths is?

Back 349

Macula; hair cells imbedded in membrane which also has otoliths imbedded; head tilt induces it to pull on the cilia

Front 350

Where is the saccule

Back 350

Just beneath the utricle, perpendicular to saccula (macula orientation)

Front 351

What is the sensory epi set up on the semicircular cannals?

Back 351

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

Front 352

Where is the vest. Ganglion, what does it connect?

Back 352

Scarpa’s ganglion in the internal aud. Meatus, has bipolar ganglion cells that innervate the hair cells and form part of 8th nerve

Front 353

What are the parts of the vestibular gangia?

Back 353

1. superior; 2. Medial; 3. Lateral; inferior → each of these has a specific set of connections with the 3rd, 4th, 6th nuclei for VOR

Front 354

Lateral vest nucl input is from?

Back 354

(Deiter’s nucleus); receives input from the macula of the utricle; sends output to the vestibulo-spinal tract mostly for the antigravity muscles

Front 355

Medial and sup get input from?

Back 355

Mostly cristae of the semi-circular cannals; axons send input to MLF [which mediate eye and neck movements]

Front 356

Inferior get input from?

Back 356

(descending vest-nucl) gets input from both semi-circ and maculi of utricle and saccule;

Front 357

Vestibular reflexes divisions?

Back 357

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

Front 358

What mediates postural reflexes

Back 358

Lateral vestibulospinal tract, mainly to gamma motor neurons which change muscle done (alpha a fair amount too); TONIC drive also gives tone to muscle

Front 359

What is the vestibulocollic reflex

Back 359

Just like VOR but for head (think chicken walk)

Front 360

What does the VOR do to muscles?

Back 360

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)

Front 361

What are the functions of the Outer, middle, inner ear?

Back 361

Outer (pinna and aud canal)- amplify and filter sounds; Middle (cavity and ossicles- amplify pressure and alow gain control; inner- cochlea

Front 362

How does the pinna amplify sound? Aud cannal?

Back 362

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)

Front 363

Why does the middle ear exits (or at least one reason)

Back 363

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

Front 364

How is gain controlled in the middle ear

Back 364

The tensor tympani muscles (analogous in fxn to pupil) which are innervated by (CN V)—maleus and incus; stapedius from facial nerve CN VII

Front 365

What is the helicotrema

Back 365

End of the basilar membrane space; connection between the scala vestibuli and scala typani

Front 366

Describe the spatial frequency on basilar mem

Back 366

Stiff at start floppy at end, related to where basilar is most deformed with differing frequencies

Front 367

Organ of Corti is?

Back 367

The name given to the sensory/motor/membranes that make sound transduction possible

Front 368

Why is sound transduced by the hair cells

Back 368

Because hair cells are deformed due to being imbedded in two types of membranes with different properties of stiff/floppy; motion opens ion channels

Front 369

Why don’t you get single ear deficits?

Back 369

There is lots of cross-talk between the ears throughout the auditory system. Therefore you don’t get deficits (lasting)

Front 370

What are the three main auditory paths?

Back 370

1. Classical- this is the most important for understanding; 2 & 3. Are interested in determining the source location of sounds

Front 371

Classical pathway

Back 371

1. spiral ganglion; 2. Cochlear nucleus→ acoustic stria and trapezoid body; 3. Inferior colliculus; 4. MGN; 5. BA 41

Front 372

What are the parts of cochlear nucleus

Back 372

The DCN → inferior colliculus (classical pathway)

Front 373

What are the divisions of the inf colliculus?

Back 373

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

Front 374

Three subnuclei of MGN

Back 374

1. dorsal→ broad tuning for frequency (no tonotopy [location?]); 2. Ventral→ primary for the classical pathway; 3. Medial → broad tuning but has tonotopic organization

Front 375

What does cortical (auditory) damage do in a human?

Back 375

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)

Front 376

What does the MSO do?

Back 376

It compares time of arrival in each ear do determine location of sound origin (for each frequency)

Front 377

Why does the LSO input from the contra ear stop off?

Back 377

It needs to be changed to an inhibitory signal, by doing this you get to compare the absolute intensity that each ear received

Front 378

What is the trade off for rods vs cones

Back 378

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

Front 379

What does light do to RM potential in cell?

Back 379

It decreases the resting membrane potential (hyperpolarizing the cells)

Front 380

What is the threshold of independent sound discrimination?

Back 380

About 1800 Hz in humans

Front 381

Which component of sound requires binaurality for effective discrimination?

Back 381

Perception of the direction of propagation to localize sounds

Front 382

What are the components of the outer ear?

Back 382

External meatus (auditory canal)

Front 383

Describe pinna function.

Back 383

Amplification and directional filtering (ear most sensitive to sounds from the front)

Front 384

Describe external auditory meatus function.

Back 384

Filtering through resonance. Especially good at amplifying frequencies between 2-6000Hz

Front 385

What kind of gain does the external ear provide?

Back 385

About 20 db

Front 386

What implications does a less versatile, smaller pinna have for human hearing?

Back 386

Amplification not as dependent on the pinna, localization not deterred

Front 387

What comprises the middle ear? What is its function?

Back 387

Tympanic membrane

Front 388

How do the ossicles provide amplification?

Back 388

Area ratio (tm: oval window, 20:1)

Front 389

How does the middle ear provide gain control?

Back 389

Action of two muscles attached to the ossicles:

Front 390

Explain auditory hypersensitivity in Bell’s palsy and/or myasthenia gravis.

Back 390

Loss of control over middle ear muscles prevent the ossicles from effectively dampening sound—can result in inner ear damage.

Front 391

What comprises the inner ear?

Back 391

Cochlea (ventral)

Front 392

Where is the sensory apparatus of the ear located?

Back 392

In the membranous labyrinth, tube contained within bony cochlea

Front 393

What is the modiolus?

Back 393

Axis of the bony spiral

Front 394

Describe the relationship of the labyrinths within the cochlea.

Back 394

Membranous labyrinth divides the osseous labyrinth into the scala vestibuli and the scala tympany

Front 395

What parts of the membranous labyrinth partition the scala vestibuli and scala tympani from the cochlear duct?

Back 395

Reisner’s membrane and basilar membrane, respectively

Front 396

What is the cochlear duct?

Back 396

Canal formed by membranous labyrinth

Front 397

Describe the path of sound from stapes to hair cell.

Back 397

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

Front 398

Where is high frequency energy best transmitted along the basilar membrane? Why?

Back 398

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.

Front 399

Where is the round window? The oval window? How does the function differ?

Back 399

The round window is at the end of the cochlea, at the end of the scala tympany. It helps dissipate the pressure waves.

Front 400

Describe changes in the displacement waves as they move down the basilar membrane.

Back 400

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.

Front 401

Described how sound frequencies are “mapped” along the length of the basilar membrane.

Back 401

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.

Front 402

What is the organ of Corti?

Back 402

Specialized epithelial structure on top oof the basilar membrane that contains the hair cells.

Front 403

What is the tectorial membrane?

Back 403

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.

Front 404

How do hair cells transduce fluid pressure energy?

Back 404

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.

Front 405

Describe the path of sound transduction by the ear.

Back 405

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

Front 406

What are the types of hair cells? What do they do? Where are they located?

Back 406

Inner hair cells located in row closest to modiolus. Sensory structures, communicate with brain via auditory neurons in nerve.

Front 407

How are inner hair cells innervated?

Back 407

By radial fibers from bipolar cells in spiral ganglion. 20 radial neurons to 1 inner hair cells.

Front 408

How are outer hair cells innervated?

Back 408

From olivocochlear bundle from contralateral superior olivary complex, mostly all direct efferent connections.

Front 409

What is characteristic frequency?

Back 409

Frequency at which a particular hair cell is responsive (tip of V)

Front 410

How do characteristic frequencies of hair cells change along the basilar membrane?

Back 410

High to low

Front 411

Describe the idea of “labeled lines”

Back 411

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).

Front 412

What is “phase-locking” and what component of sound does it encode?

Back 412

Encodes “timing” of acoustic events.

Front 413

How is sound intensity encodes?

Back 413

Firing rate of individual neurons or by the number of activated fibers.

Front 414

How does the frequency range that a particular hair cell responds to, change with increasing amplitude?

Back 414

The range becomes larger

Front 415

How does the rate of firing change at the beginning and at the end of an auditory event?

Back 415

Dramatic increase in firing at the beginning, drop off (below basal activity) when it ends.

Front 416

What is tonotopy?

Back 416

Systematic arrangement of neurons according to their frequency tuning

Front 417

Why is there such extensive bilateral convergence in the auditory system?

Back 417

Sound localization

Front 418

Describe “step 1” in the auditory system, from cochlea to brain stem.

Back 418

Bipolar neurons (cell bodies in spiral ganglion) relay signal from hair cells in cochlea, through auditory nerve, intl brain stem.

Front 419

Describe the course of auditory nerve fibers from the brain stem cochlear nucleus to the inferior colliculus.

Back 419

Fibers from cochlear nucleus decussate in the acoustic stria and trapezoid body

Front 420

Where does the lateral lemniscus send collaterals as it ascends to the inferior colliculus?

Back 420

Superior olivary complex

Front 421

In what tracts do fibers from the cochlear nucleus cross the brainstem?

Back 421

Acoustic stria

Front 422

From where does the inferior colliculus receive projections? What is its function?

Back 422

Lateral lemniscus (from cochlear)

Front 423

To where does the inferior colliculus project?

Back 423

Contralateral inferior colliculus

Front 424

Where does the medial geniculate nucleus project?

Back 424

To auditory cortex

Front 425

What is are the auditory radiations?

Back 425

Projections from MGN to auditory cortex

Front 426

What are the components of the cochlear nucleus? How are the fibers organized?

Back 426

Dorsal (DCN)

Front 427

What different cell types are contained within the three tonotopic subdivisions of the cochlear nucleus?

Back 427

DCN—fusiform, “pausers”

Front 428

How do pausers, primary-like, and onset neurons function?

Back 428

Pausers, respond with few spikes at onset of auditory stimulation, pause, then train of spikes for duration of stimulus

Front 429

Secondary cells of the auditory processing system are contained within which structure? Give three examples.

Back 429

Cochlear nucleus:

Front 430

Where does the DCN project?

Back 430

Pauser cells project to contralateral inferior colliculus

Front 431

Where do onset cells project? From which region of the cochlear nucleus?

Back 431

Onset cells project to pontine nuclei (then to inferior colliculi)

Front 432

Where do AVCN cells project? What type of cells are these?

Back 432

Primary like cells project to the pontine nuclei

Front 433

What are the direct and indirect pathways in acoustic processing? Which nuclei and cell types are involved?

Back 433

Direct. From DCN to contralateral inferior colliculus. Pauser cells.

Front 434

What function does the direct pathway have and how is this different from the indirect pathway?

Back 434

The direct pathway is likely involved in sound identification while the indirect pathway integrates binaural information and contributes to sound localization

Front 435

What are two binaural cues?

Back 435

Interaural intensity differences

Front 436

What is IID and what is the threshold for human detection?

Back 436

Interaural intensity differences. Idea that contralateral ear detects a lower intensity sound.

Front 437

What is ITD, what is the human threshold? How does this compare with the duration of an action potential?

Back 437

Interaural time differences.

Front 438

Which structure seems to be primarily responsible for binaural stimuli integration? Which nuclei contribute?

Back 438

Pontine nuclei

Front 439

What is the initial site for IID detection? What inputs does it receive?

Back 439

Lateral superior olive

Front 440

What is the NTB? Where does it project? What information does it receive? What kind of output does it have?

Back 440

Nuclei of the trapezoid body

Front 441

How does the LSO encode IID information?

Back 441

Particular neurons have different selectivity for various IID, received from the AVCN and the NTB

Front 442

Where is binaural time comparison occur?

Back 442

Medial superior olive

Front 443

Describes the composition of the MSO.

Back 443

Ribbon of spindle-shaped cells with two primary dendrites (medial and lateral)

Front 444

Where do inputs from the ipsilateral AVCN go (in the MSO)?

Back 444

To the lateral dendrites.

Front 445

Medial dendrites of MSO neurons receive information from ___?

Back 445

Contralateral AVCN

Front 446

How is the inferior colliculus divided?

Back 446

Central

Front 447

Where does the classical ascending pathway project?

Back 447

Central nucleus of the inferior colliculus

Front 448

What projects to the pericentral, external, and central nucleus of the inferior colliculus?

Back 448

Pericentral—strong descending projection from auditory cortex

Front 449

What region integrates SS and acoustic inputs?

Back 449

External nucleus of the inferior colliculus

Front 450

Which nucleus contains neurons with a well defined CF and sharp frequency tuning?

Back 450

Central nucleus

Front 451

How are frequencies represented in the central nucleus of the inferior colliculus?

Back 451

Tonotopically (low dorsal, high ventral)

Front 452

What nuclei comprise the MGN? Which is involved in the “classical” pathway?

Back 452

Dorsal

Front 453

From where do the other regions receive information?

Back 453

Dorsal—pericentral nucleus

Front 454

Which MGN nuclei are tonotopically organized?

Back 454

Ventral and Medial

Front 455

What BA is the primary auditory cortex? What are its inputs/outputs?

Back 455

Area 41

Front 456

Describe the different dimension of organization in the primary auditory cortex.

Back 456

Tonotopic bands (medial high frequency→)

Front 457

Where are other auditory fields located? What is their function?

Back 457

Belt around AI

Front 458

What are the connections of AII?

Back 458

Reciprocal with Dorsal MGN and project to pericentral nucleus of inferior colliculus

Front 459

Describes the classical pathway.

Back 459

Central nucleus of inferior colliculus→ ventral of medial geniculate→A1 of auditory cortex

Front 460

Alternative pathway.

Back 460

Pericentral nucleus of inferior colliculus->dorsal MGN→AII of auditory

Front 461

What defects does a cortical lesion have on auditory function?

Back 461

Sound localization and recognition of temporal sound patterns

Front 462

Medial geniculate

Back 462

CN: DCN, AVCN, PVCN

Front 463

Be able to draw pathways

Front 464

What type of image do the cornea and lens produce on the retina?

Back 464

Real, inverted image

Front 465

What types of photoreceptors does the human eye contain (two types and then subtypes)?

Back 465

Rods

Front 466

What is the fovea? What photoreceptors are located here?

Back 466

Central portion of the visual field

Front 467

What properties of the photoreceptors allows for such high visual acuity in the fovea?

Back 467

Cones are thinner, allowing for denser packing, and smaller area: cone ratio

Front 468

What accounts for the “pit-like” appearance of the fovea?

Back 468

Other cells between the light source and the photoreceptors are pushed aside to reduce light scattering

Front 469

Where are rods located? How might this affect how one looks at dim light and why?

Back 469

Mostly in periphery

Front 470

What are the three segments of a photoreceptor? What are the basic contents/function of each segment?

Back 470

Outer segment: visual pigment molecules, responsible for absorbing light and generating the electrical signal

Front 471

How does the structure of the photosensitive membranes in rods and cones differ?

Back 471

Rods. Series of intracellular discs, surrounded by a separate outer envelope.

Front 472

What are pigment epithelial cells? What is their function?

Back 472

Epithelial cells on back of eye, in contact with photoreceptors

Front 473

Where are melanin granules located? What do they do?

Back 473

Located in pigment epithelial cells

Front 474

Describe turnover of the outer segments.

Back 474

Discs are continuously made and shed from the tip of the outer segment.

Front 475

Describe the structure of visual pigments in rods and cones.

Back 475

Similar structure in both. Protein portion and a chromophore, 11 cis-isomer of vitamin A (retinal)

Front 476

What is the general structure of the rod pigment?

Back 476

Rhodopsin contains opsin (7 transmembrane protein) and chromophore (retinal) that lies between the helices of opsin

Front 477

Why does rhodopsin appear to be red? How does this property correspond with the ability to see dim light?

Back 477

Absorbs light near 500 nm, which is bluish-green

Front 478

What happens when retinal (bound to the protein) absorbs light?

Back 478

11-cis→ all-trans form producing metarhodopsin II. Involves activation of G-protein cascade, all-trans retinal released from opsin by hydrolysis

Front 479

What are the light reactions in the phototransduction cascade?

Back 479

Photoisomerization of retinal from 11-cis to all-trans

Front 480

What are dark reactions?

Back 480

The reactions following photoisomerization of 11-cis retinal that proceed spontaneously

Front 481

What does it mean that light “bleaches” rhodopsin?

Back 481

Light causes photoisomerization of retinal to all-trans form which is eventually cleaved from the opsin molecule.

Front 482

How does the photoreceptor “unbleach”?

Back 482

11-cis is regenerated enzymatically and spontaneously rejoins opsin

Front 483

What proteins are involved in the light-activated signal transduction pathway? What do they do?

Back 483

Metarhodopsin II (all-trans retinal-opsin) stimulates transducin (GTP-binding protein)→ activates cGMP phosophdiesterase→ hydrolysis of cGMP→ closes cGMP-gated cationic channels

Front 484

What is the end result of cGMP hydrolysis?

Back 484

Closing of cGMP-gated cationic channels

Front 485

What happens when metarhodopsin II binds transducin?

Back 485

Exchange of GDP for GTP, resulting in activation of cGMP PDE

Front 486

Describe the deactivation of the phototransduction pathway.

Back 486

Metarhodopsin II is phosophorylated by rhodopsin kinase and binding of arrestin

Front 487

Alpha-subunit of transducin?

Front 488

What is “bradyopsia”? What can cause it?

Back 488

Slow vision, diminished visual acuity for moving objects

Front 489

What is the polarization state of the outer segment in darkness? In lightness? What causes this?

Back 489

Dark: depolarized, cationic channels open

Front 490

How is stimulus strength encoded by photoreceptors?

Back 490

Response amplitude

Front 491

What is the threshold of stimulation that will result in photoreceptor hyperpolarization? What is required for conscious perception of light?

Back 491

1 photon

Front 492

What is thermal isomerization of rhodopsin and how does this relate to dim light perception and the stability of rhodopsin?

Back 492

Thermal isomerization is the decay of rhodopsin. Since it is indistinguishable from light-mediated bleaching, sets a limit on ability to perceive dim light

Front 493

How do the synapses of photoreceptors onto horizontal and bipolar cells differ from regular synapses?

Back 493

Ribbon synapses, contain 100s of vesicles and release increases steadily as function of membrane production

Front 494

What is the NT released by photoreceptors and how does light affect this release?

Back 494

Glutamate

Front 495

What types of glutamate receptors are involved in the post synaptic response and how does this define bipolar cell types?

Back 495

Metabotropic→ depolarization→ “On” cells

Front 496

How do on and off cells respond to light?

Back 496

On cells (metabotropic) depolarize in light

Front 497

What are other names for on and off bipolar cells?

Back 497

D and H bipolar cells

Front 498

How is the retina organized?

Back 498

Photoreceptors and horizontals to bipolars and horizontals in outer plexiform layer

Front 499

What are amacrine cells? Where are they located and what are inputs/outputs?

Back 499

Diverse group of neurons forming the inner plexiform layer

Front 500

What is the “direct path” in the retina?

Back 500

Photoreceptor→ bipolar→ RGC

Front 501

What are the different types of bipolar cells, other than “on” or “off”?

Back 501

Rod bipolars (receive input from multiple rods)

Front 502

Similarly, what are the different types of RGCs?

Back 502

Midget ganglion cells (usu 1 midget bipolar)

Front 503

How does the spatial resolution of parasol cells related to that of midget cells?

Back 503

Lower spatial resolution

Front 504

Which NTs are released by the retina (and by which cells)?

Back 504

Glutamate: rods, cones, bipolars

Front 505

What are interplexiform cells?

Back 505

Neurons that relay info from inner layers of retina back to horizontal cells in outer plexiform layer

Front 506

How does a horizontal cell respond to light? What type of stimulus is best to activate this response?

Back 506

Graded hyperpolarization

Front 507

What is a receptive field?

Back 507

Region of retina that influences the activity of a cell when stimulated by light

Front 508

What is a receptive field “surround”?

Back 508

Region around center of receptive field that gives opposite response to light (than center)

Front 509

Why would a light falling on both the center and surround of a receptive field elicit any bipolar cell response?

Back 509

B/c surround signals are delayed by traveling through additional synapse

Front 510

What type of stimulus that most depolarized the Off-bipolar?

Back 510

Dark spot on bright background

Front 511

How do negative feedback synapses regulate surround of receptive fields in bipolars? What cell types is responsive to this?

Back 511

Horizontal cells modulate response of photoreceptors presynaptically.

Front 512

Why do bipolar cells have center surround receptive fields?

Back 512

Important form of data compression that gives more significance to points of contrast rather than intensity at every point

Front 513

What is spatial contrast?

Back 513

Degree to which a region is brighter or darker than surrounding regions

Front 514

Most ganglion cells carry which type of information?

Back 514

Most have center-surround receptive fields, so carry information about spatial contrast

Front 515

How is surround receptive field mediated for retinal ganglion cells?

Back 515

Response of bipolar cells (on-bipolar cells antagonized by light in surround)

Front 516

What are two major classes of ganglion cells?

Back 516

Magnocellular (parasol), respond transiently and have larger receptive fields, spatial and temportal contrast

Front 517

What is univariance? How does this apply to color processing?

Back 517

Any receptor with a single binding site cannot encode identity of ligand (wavelength) separately from concentration of ligand (intensity)

Front 518

What is an action spectra?

Back 518

Measurements based on light responses

Front 519

Describe structure of the three cone pigments.

Back 519

Similar to rhodopsin. 7-tm protein, with chromatophore

Front 520

What is protanopia?

Back 520

Red-pigment lacking color blindness

Front 521

What is deuteranopia?

Back 521

Green-pigment deficient color blindness

Front 522

What is tritanopia?

Back 522

Blue-cone lacking color blindness

Front 523

Which is the most rare?

Back 523

Tritanopia

Front 524

What is anomalous trichromacy?

Back 524

Trichromatic but have a mutation which shifts the absorption spectrum of one of the pigments

Front 525

What is achromatopsia? What causes this?

Back 525

Failure to see colors but not patterns, with normal cones

Front 526

How might one view the color red given non-white illumination?

Back 526

Computation of “reflectance” from ratio of reflect and incident spectral intensities

Front 527

What are double color opponent cells? Where are they located?

Back 527

Located in parvocellular layer of LGN

Front 528

Chapter 27: Visual System I

Front 529

What are scotomas?

Back 529

Regions of blindness in the visual field

Front 530

What is diplopia when does it happen?

Back 530

It is double vision; it occurs for multiple reasons the most important being the fact that CN or CN nuclei are damaged

Front 531

What parts of each eye does the R monocular hit

Back 531

R monocular hits L temporal and R nasal

Front 532

Describe path of visual information starting at fovea (to cortex exclude brainstem stopoffs)

Back 532

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

Front 533

Describe other light pathways

Back 533

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

Front 534

What optic N. called after chiasm?

Back 534

Optic tract- it not has information from only one hemi-field

Front 535

Right optic tract cut deficit

Back 535

Both eye L visual hemi-field= L homonymous hemianopsia

Front 536

Thalamo-cortical path is responsible for (cognitive)

Back 536

The things we normally associate with vision, perception, object recognition, depth perception, color vision

Front 537

stimulate sup colic in monkey what happens

Back 537

You evoke saccadic eye movements, important as it is subconscious, brings eyes to interesting things (e.g. flash)

Front 538

What is E-W input, output and action

Back 538

Input is from the pretectal nucleus which somehow calculates light intensity; output Is parasympathetic to the ciliary ganglion→ iris sphincter muscles to constrict

Front 539

Which layers are contralateral in LGN; who cares?

Back 539

1/4/6; I remember 1+4 = 5 is contra

Front 540

One possible function of LGN?

Back 540

To ensure that visual information from each eye is precisely aligned before being sent to the cortex

Front 541

Which layers ore P & M

Back 541

1 & 2 are M; 3→ 6 are P and carry color information and center surround info

Front 542

What are the M cells good at then?

Back 542

They are very good at timing issues, where as P are not→ nor is the downstream cortical area

Front 543

What is the koniocellular pathway

Back 543

This is a new (ish) path that carries blue info to the cortex; it is between the other LGN layers

Front 544

Why synapes at LGN if no info transformed?

Back 544

It receives input from cortex and probably acts as a gate; (from fact that only 10% of synapses are LGN, rest cortex)

Front 545

History note→

Back 545

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)

Front 546

How is info transformed at cortical level

Back 546

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

Front 547

What are the exceptions to orientation select

Back 547

Some V1 cells have receptive fields that are the same as LGN (on off center cells)→ maybe important for timing?

Front 548

What are the two main cells types in V1?

Back 548

Stellate and pyramidal cells; most stellate are in layer IV, most pyramidal are in 2,3,5,6

Front 549

What are the response prop in other than layer 4

Back 549

They are complex in general, and send their output to other cortical areas

Front 550

How is orientation selectivity organized

Back 550

Orientation colums (cortical layers 1-6) all respond best to the same line orientation

Front 551

As you travel across cortex how does orientation select change?

Back 551

1 & 2 columns; 3 shows that orientation selectivity smoothly changes from column to column (can hit 90 degree switches though)

Front 552

How quick does the change occur (distance)

Back 552

About 10 degree change every 25-50μm (180 degrees/ 0.5-1 mm)

Front 553

Hubel and Wiesel thought it was a grid, but how is it really?

Back 553

Not layed out in a grid, more complex, but the idea is the same

Front 554

What are CO blobs what do they do?

Back 554

CO blobs are the regions that get color information in V1 and are insensitive to orientation

Front 555

What does each square mm of cortex contain

Back 555

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

Front 556

Where are the binocular cells?

Back 556

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

Front 557

In general what does the striate cortex do?

Back 557

1. efficiently represents important features (lines etc); 2. Unifies both eye input; 3. Functional architechture for line orientation

Front 558

What is extrastriate visual cortex?

Back 558

Cortex outside of V1 that deals with vision, but is processing higher level (more complex/abstract) representations

Front 559

What are the 2 main visual pathways

Back 559

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)

Front 560

What is blindsight

Back 560

Ability of people (without conscious perception) to act correctly on visual stim, mediated by sup colic

Front 561

What does visual agnosia mean

Back 561

“agnosia” not knowing

Front 562

Apperceptive agnosia

Back 562

These people cannot copy; can’t recognize due to more visual deficits

Front 563

Associative agnosia

Back 563

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.

Front 564

What is extinction

Back 564

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)

Front 565

What is ventral simultagnosia?

Back 565

Patients have difficulty perceiving multiple objects (no matter where they are in space)

Front 566

Cerebral akinotopsia

Back 566

These patients have difficulty sensing motion, and is often from damage that includes the posterior middle temp gyrus (like MT)

Front 567

Cerebral achromatopsia

Back 567

Inability to precieve color (usually damage is unilateral, as is the deficit)→ associated damage: inferior occipitotemporal cortex BA 37/19

Front 568

Prosopagnosia

Back 568

Iniability to recognize faces, in this deficit you selectively loose the ability to distinguish familiar objects (faces, birds (if a birder), goats, etc.)

Front 569

Monkey studies and lesion location object vs. landmark

Front 570

Monkey MT does

Back 570

Motion; receives input from the direction selective cells; think cerebral akinotopsia

Front 571

V4

Back 571

Color area (think cerebral achromatopsia); fine discrimination; major output is to temporal areas “what” path

Front 572

Attention influence general principals

Back 572

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

Front 573

What (again) are the input layers of cotex

Back 573

4c alpha & 4 c beta

Front 574

Neglect in humans

Back 574

“Oh I missed something on that page? It must be on my left I guess.”

Front 575

Define sleep

Back 575

1. little movement; 2. Stereotypic posture; 3. Reduced response to ext. stim; 4. And it is reversible

Front 576

What are the EEG properties of wake

Back 576

Low voltage fast (16-25 Hz) ossilation

Front 577

Sleep stages and EEG findings

Back 577

Stage 1: EEG decreases, EOG slow rolling eye movements, theta waves 3-7 Hz

Front 578

What is the sleep cycle and progression

Front 579

Sleep onset and consequences

Back 579

Retrograde amnesia→ can’t remember a phone call or page in night, sleep deprived can enter REM directly,

Front 580

How does sleep change as we age

Back 580

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)

Front 581

How is motor activity inhibited during REM

Back 581

By the pontis oralis inhibitory connections to the ventromedial medullary reticular formation

Front 582

Important edocrine changes

Back 582

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

Front 583

What does the pontine locus coeruleus do? Who else does this

Back 583

Stimulates wakefulness; also by 1. Midbrain dorsal raphe nuclei; 2. Tuberomamilary nucleus, basal forbrain, lateral dorsal tegmentum,

Front 584

How is NREM mediated

Back 584

Active inhibition of most of the neurons in the hypothalamus, temp may mediate this

Front 585

How is REM mediated?

Back 585

Cholinergic neurons in the basal forbrain, lateral dorsal tegmentum and pedunculopontine nuclei are active during REM

Front 586

What do high/low amplitude EEG signify

Back 586

High amp signifies synchrony it has nothing to do with activity low equals asynchronous→ likely from thalamocortical oscillations

Front 587

Insomnia means

Back 587

Difficulty initiating or consolidating sleep (20-33% of people have), shor sleep time, or non-restorative sleep

Front 588

Narcolepsy

Back 588

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)

Front 589

Apnea 2 kinds

Back 589

1.

Front 590

2.

Back 590

central → CHF and premature/ young infants possibly because BStem isn’t mature

Front 591

Parasomnias

Back 591

Movements and behaviours occurring during sleep; sleepwalking, night terrors, RLS

Front 592

Facts about sleepwalking

Back 592

First third of night; 15 seconds →30 min; sitting, standing, walking, fumbling with objects

Front 593

RLS

Back 593

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

Front 594

Night terrors

Back 594

Stage 3 & 4 sleep most common in children; terrified and scream; sleep terrors are usually not remembered

Front 595

REM sleep behavior disorder

Back 595

Man fights wolf from eating wife→ really hitting wife

Front 596

Physiologic changes in sleep

Back 596

1. active heat loss; lower volume more concentrated urine; less digestion; decreased responsivity to senses

Front 597

What does sleep do to TSh levels

Back 597

It actively suppresses TSH thereby decreasing metabolism

Front 598

What are the 3 main stages of dev?

Back 598

1. neuron generation (neurogenesis); 2. Extend axons (pathway/target selection); 3. Selecting the correct connections (address selection)

Front 599

Where is the zone of proliferation?

Back 599

Near the ventricles→ cells here divide and eventually give rise to the whole nervous system

Front 600

Interkinetic nucl migration

Back 600

The progression from G1 → mitosis and the location that each timepoint the cell portray (diagramed above)

Front 601

What is the order of cell generation

Back 601

From the inside out (later neuons must migrate through previous layers to get to their specific spot)

Front 602

How is position related to generation time?

Back 602

The early time points end up in earlier layers (6 & 5) that the ones that divide later “birthdating”

Front 603

What does a radial glia do?

Back 603

Provides a guide to the migrating neuron

Front 604

Why design a system where the cell has to move?

Back 604

In this way the cell can sense the environmental signals and determine what type of cell to become

Front 605

When are neurons and glia made

Back 605

In general neurons are made first, once this is complete the glia are made, tumors may arise from these remaining NSC in the SVZ

Front 606

What happens to the radial glia after dev

Back 606

The radial glia actually degenerate

Front 607

How do cells (in layers) know what to become?

Back 607

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.

Front 608

How do NSC know to make glia

Back 608

Neurons make glial growth factor with inhibits NSC from making neurons, then they make glia

Front 609

How are axons guided?

Back 609

axons have growth cones →

Front 610

What are guidpost cells

Back 610

Just what they sound like, they are waypoints that the cell has to pass in order to reach its destination

Front 611

What is required for early circuitry development?

Back 611

Molecular cues, but the later fine circuitry development is based upon activity

Front 612

What is the visual critical period?

Back 612

The idea that correct vision (no strabismus cataracts etc) is required to accurately prune and finalize the circuit

Front 613

What happens if you cover an eye during critical period?

Back 613

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]

Front 614

What does the above test tell you?

Back 614

That stimulation is required for normal wiring; that if quiet, adjacent areas make stronger connections and use the “unused” cortex

Front 615

So what mechanism explains this phenomenon

Back 615

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

Front 616

How could you prove activity is required?

Back 616

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

Front 617

At the cellular level how could competition change wiring?

Back 617

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]

Front 618

Why does this competition lead to lasting structural changes?

Back 618

The cells during the critical period are competing for limited resources (neurotrophic factors); when they don’t get enough they retract

Front 619

What can this competition allow?

Back 619

It can allow the matching of the number of pre & post synaptic terminals

Front 620

Glia make up __% of brain cells

Back 620

90% of cells, but because they are smaller about 50% of volume

Front 621

What are the two main classes of glia

Back 621

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

Front 622

What is know about the fxn of astrocytes

Back 622

Both have end-foot dilations that contact and surround the capillaries and arterioles throughout the brain (BBB); they also envelope synapses

Front 623

What are the two types of astrocytes

Back 623

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

Front 624

What are the two types of oligos?

Back 624

1.

Front 625

2.

Back 625

interfasicular- white matter

Front 626

What do perineuronals do

Back 626

Adhere to somas of neurons (not myelinating)… the might actually be microglia and not astrocytes (unknown)

Front 627

And interfasicular

Back 627

Myelinate axons from 1-30 of them

Front 628

What are the main proteins in myelin

Back 628

1. proteolypid protein (PLP)-- transmembrain; 2. Myelin basic protein (MBP)—cytoplasmic

Front 629

Where/when do glia develop

Back 629

They develop in the SVZ following neurons; they also migrate along the radial glia

Front 630

What controls oligo dev? And why is the number perfect for myelination?

Back 630

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)

Front 631

What happens to the others?

Back 631

They undergo apoptosis (about 2x as many are mad as are needed)

Front 632

What is distinct about glia membrane properties vs neurons

Back 632

No dendrites; axon; or synapes; -90 mV resting membrane potential; therefore primarily permeable to K+

Front 633

Why can K+ be taken up by glia? What is it called?

Back 633

K+ can be taken up b/c of nernst equation; therefore the glia “buffer” by quickly taking up K+

Front 634

What do astrocytes do?

Back 634

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)

Front 635

What happens to neurons w/o glia?

Back 635

You can form synapes (but low #) and they are 100 times less active

Front 636

What are the different types of memory?

Back 636

Declarative (explicit/episodic/recent) memory

Front 637

What is declarative memory?

Back 637

Memory that mediates conscious recollection of events and facts

Front 638

How can declarative memory be tested?

Back 638

Presentation of words/items to remember, and after a delay ask to recognize or recall items

Front 639

What type of memory is impaired in global amnesia? What is global amnesia?

Back 639

Declarative memory

Front 640

What sort of lesion characterizes anterograde amnesia?

Back 640

Medial-temporal brain regions (HM) or

Front 641

What sort of lesion did HM have?

Back 641

Bilateral medio-temporal lobectomies

Front 642

What is Korsakoff’s syndrome?

Back 642

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

Front 643

How might unilateral medio-temporal lobe or diencephalic damage present?

Back 643

As material-specific amnesia (left-sides with learning verbal material, right-sided with learning nonverbal material)

Front 644

What lesion might result in an inability to learn new verbal material?

Back 644

Due to a left sided medial-temporal or diencephalic lesion

Front 645

What evidence is there that medial temporal lobe structures are not involved in storage of long term memory?

Back 645

HM did not have retrograde amnesia, must mean that those memories are stored elsewhere. However, MT lobe is important for consolidation of declarative memory

Front 646

In what disease is there progressive damage to entorhinal and hippocampal brain regions? What type of memory does this impair?

Back 646

Alzheimer’s disease

Front 647

Developmental abnormalities are common to which two disorders?

Back 647

Schizophrenia

Front 648

What region may be important for emotional aspects of memory?

Back 648

Amygdala

Front 649

What is procedural memory?

Back 649

Memory that mediates forms of skill learning

Front 650

How is procedural memory measured?

Back 650

By progressive improvements in speed or accuracy by a subject across different sessions

Front 651

What is classical conditioning? To which type of memory is it most closely related?

Back 651

Association learning between some unconditioned stimulus with an unconditioned response to form a conditioned response

Front 652

What type of memory is frequently impaired in individuals with basal ganglia disease? What are three examples?

Back 652

Usually skill learning (procedural memory)

Front 653

What types of learning/memory are impaired with cerebellar disease?

Back 653

Skill learning and classical conditioning (procedural memory)

Front 654

What is repetition priming?

Back 654

Change in speed, accuracy, or bias with which repeated stimuli are processed relative to either their initial processing or some baseline

Front 655

Do most amnesiac patients have normal or abnormal repetition priming?

Back 655

Normal

Front 656

What is perceptual priming?

Back 656

Form specific processes involved in stimulus identification

Front 657

What is conceptual priming?

Back 657

Meaning-related processes involved in stimulus comprehension

Front 658

Plasticity in modality-specific input cortices (like visual, auditory, etc) is demonstrated with which kind of priming?

Back 658

Perceptual priming

Front 659

Which type of priming is associated with multi-modal (association) cortices?

Back 659

Conceptual priming

Front 660

Repetition priming is associated with more or less activation in cortical regions?

Back 660

Less

Front 661

What is working memory?

Back 661

Mnemonic processes involved in temporary storage of information being presently used

Front 662

What are “memory buffers”

Back 662

Refer to areas of brain that hold information

Front 663

What are executive working-memory processes?

Back 663

Hold goal-oriented information in mind and guide mental and motor action

Front 664

Where are the executive working-memory regions located?

Back 664

Prefrontal neocortex

Front 665

What type of memory processes are important for strategic memory performance?

Back 665

Executive working memory

Front 666

Why might HD or PD patients have trouble with executive working memory deficits?

Back 666

Frontal lobes may be impaired or basal ganglion may play a role (b/c of communication with frontal lobe structures)

Front 667

Is working memory the path to long term memory?

Back 667

No. These are actually processed in parallel.

Front 668

In the most general sense what is aphasia?

Back 668

It is a disturbance in the ability to understand or produce speech (but not motor deficits) e.g. grammar/syntax

Front 669

Can deaf (signers) get aphasia?

Back 669

Yes; therefore this machinery isn’t simply for sound interpretation but for grammar and syntax

Front 670

What is syntax

Back 670

The grammatical structure of sentences

Front 671

What are language issues based on motor problems called?

Back 671

Dystarthria→ this is important because dysarthria leaves language comprehension completely intact

Front 672

How is the language circuit conceptualized now

Back 672

A series of regions that perform functions on the material and form bidirectional communication (neural network)

Front 673

What does a broca’s aphasic sound like

Back 673

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?

Front 674

Wernicke’s aphasia

Back 674

Speech is fluent (in that it is effortless sounding), but utterly meaningless; they make lots of paraphasias

Front 675

What is a paraphasia? Who cares

Back 675

When you select the wrong word for your meaning, there are semantic- ocean vs pond apple vs lemon

Front 676

Global aphasia

Back 676

Usually from and M1 occlusion of the MCA (whole L hemisphere) person can’t really comprehend or produce

Front 677

What is sham rage?

Back 677

Characteristic set of behaviors elicited by removal of the neocortex and dorsal part of diencephalons (in cats)

Front 678

Stimulation of the VM hypothalamus may lead to what types of behaviors (in cats)?

Back 678

Defensive behaviors

Front 679

Stimulation of the L hypothalamus may lead to what types of behaviors (again, cats)?

Back 679

Attack behaviors

Front 680

Describe the Papez circuit

Back 680

Major connection between hypothalamus to cortex: through mamillary bodies to anterior thalamus to cingulate gyrus

Front 681

What are the major components of the limbic system?

Back 681

-amygdala

Front 682

What is Kluver-Bucy syndrome?

Back 682

Results from bilateral temporal lobe ablations

Front 683

What does Kluver-Bucy indicate for the role of limbic structures?

Back 683

Lots of things: in particular that may be involved in selective attention (esp amygdala)

Front 684

Lesions of which area produce an increase in sham rage/aggression?

Back 684

Septal nuclei

Front 685

Where are benzodiazepines most effective at inducing their anxiolytic effects?

Back 685

In the amygdala

Front 686

What is the primary site of action of cocaine and amphetamines?

Back 686

At the nucleus accumbens (DA-ergic inputs from VTA)

Front 687

What are the primary drug actions of cocaine and amphetamine

Back 687

Cocaine: block reuptake of DA

Front 688

What is the primary site of action of opiates?

Back 688

VTA

Front 689

Review the paths to and from the amygdala and hippocampus.

Front 690

Where is the amygdala located?

Back 690

Deep to the medial surface of the temporal lobe

Front 691

What are the different amygdalar nuclei?

Back 691

Corticomedial group (cortical, medial, central nuclei)

Front 692

What are the afferents to the central nucleus?

Back 692

From other limbic structures: septal nuclei, VMH

Front 693

What are the afferents to the basolateral amygdala?

Back 693

Limbic: cingulated cortex, DM and intralaminar thalamus

Front 694

What are the two major efferent amygdalar tracts?

Back 694

Stria terminalis: VM and medial preoptic hypothalamus)

Front 695

What are other connections from the amygdala?

Back 695

Direct projection to prefrontal cortex

Front 696

What comprises the hippocampal formation?

Back 696

Hippocampus, dentate gyrus, subiculum, entorhinal cortex

Front 697

Describe the cortical composition of the hippocampal formation

Back 697

Allocortex. Hippocampus and dentate have archicortex (three layered) while entorhinal is six layered. The subiculum shows the transition from 3→6 layers

Front 698

What is ammon’s horn?

Back 698

Hippocampus proper

Front 699

Describe the internal connections of the hippocampal formation.

Back 699

Most inputs to formation go to entorhinal

Front 700

What are the perforant pathways?

Back 700

Projections from entorhinal cortex to the granule cells in the dentate gyrus

Front 701

What type of fibers project from the granule cells of the dentate gyrus to Ammon’s horn? What cell type do they terminate on?

Back 701

Mossy fibers

Front 702

What are the most prominent cell type of the dentate gyrus?

Back 702

Granule cells

Front 703

What does CA refer to?

Back 703

Cornu ammonis

Front 704

What are CA-4 and CA-3 projections called? Where do they go to?

Back 704

Schaeffer collaterals

Front 705

Where do cells of the hippocampal commissure originate?

Back 705

Dentate gyrus and ammon’s horn

Front 706

What is the psalterium?

Back 706

Fiber tract of hippocampal commissure

Front 707

How do inputs to entorhinal cortex compare with inputs to the amygdala?

Back 707

Entorhinal inputs are from the association cortices and represent polymodal sensory areas

Front 708

Where do the efferents from the subiculum go?

Back 708

To the fornix (anterior thalamus, mamillary bodies, cingulated cortex)

Front 709

What extrinsic connections project to areas of the formation outside of the entorhinal cortex and subiculum?

Back 709

Locus coeruleus and Raphe nucleus to ammon’s horn

Front 710

What are the components of the septal region?

Back 710

Lateral and medial septal nuclei

Front 711

Name the major septal nuclei efferents

Back 711

Amygdale and hippocampal formation and anterior and DM thalamus

Front 712

What are the major afferents of the septum?

Back 712

Input from reticular system: raphe, locus coeruleus, substantia nigra

Front 713

Which hypothalamic area sends diffuse projections all over the neocortex?

Back 713

Lateral hypothalamus

Front 714

Lecture 36: fMRI

Front 715

What is the basis for BOLD

Back 715

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

Front 716

What does increased signal mean in fMRI?

Back 716

It means the area is engaged in processing, but has no information as to whether or not it is required for a specific function

Front 717

DTI

Back 717

Measures white matter tracts (diffusion tensor imaging) looks at restricted (spatially) diffusion of H2O

Front 718

Diffusion clinical reason

Back 718

Clinically this is the most important scan for stroke. It is sensitive within minutes to the decoupling of metabolism and restricted diffusion

Front 719

What does the anatomy of the corpus callosum (CC) tell you about function

Back 719

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)

Front 720

What is “a” main function for the CC

Back 720

Inerhemispheric transfer of information

Front 721

How does one communicate with the R hem

Back 721

Use as little verbal information as possible

Front 722

What is the R hem good at?

Back 722

Spatial manipulation and other nonverbal skills