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159 Cards in this Set
- Front
- Back
paleocortex
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primary olfactory cortex, a layer of primitive cortex
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archicortex
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hippocampal formation layer of primitive cortex
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neocortex
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third layer of primitive cortex, contains 6 layers of its own
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layers III and V of neocortex
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output neurons that contribute to axons of underlying white matter
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layers II and IV of neocortex
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contain interneurons, dentrites from III and V, and myelinated input from thalamus and other cortical areas
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motor association areas
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1. premotor area
2. frontal eye fields 3. motor speech area of Broca 4. supplementary motor area |
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4 distinctly human traits
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1. complex language
2. precision movements of the hands and eyes 3. incredible memory storage 4. the power of forethought |
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4 pieces of indirect evidence that neocortex is involved with higher thought processing
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1. degeneration of cortex = destruciton of memory and intelligence (Alheimer's)
2. lissencephalic infants = severe mental retardation/fatal 3. animals have less cortex = less intelligent 4. more cortex in more intelligent animals |
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gestational time of neuronal development
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1 mo- no brain
2 mos- 1 cm of brain 4 mos- neocortex appears 7 mos- very developed, i guess |
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EPILEPSY
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*periodic and unpredictable seizures
*hyderexcitable and hypersynchronous brain *epileptic focus = starting pt *brain slice experiments |
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ALZHEIMER'S
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*form of dementia
*neocortex shrivelled *cholinergic neurons from basal forebrain to neocortex/hippocampus die *neurofibrillary tangles and amyloid plaques |
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epileptic focus
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starting point of seizure that spreads to otehr areas
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neurofibrillary tangles
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shrunken neural processes get tangled
-Alzheimer's |
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amyloid plaques
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junk outside tangles = detrimental to brian fxn
-Alzheimer's |
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3 ways to study fxn of association cortex
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1. lesion studies
2. monkey studies 3. fMRI imaging studies (and PET) |
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FXNS OF PARIETAL ASSOCATION CORTEX
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*understanding sensory information
*contralateral neglect syndrome |
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FXNS OF TEMPORAL ASSOCIATION CORTEX
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*(r)face recognition/(l)language
*recognizing complex images |
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FXNS OF FRONTAL ASSOCIATION CORTEX
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*behaviour
*social skills *planning |
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contralateral neglect syndrome
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lesion in one hemisphere's parietal assoication cortex
-can't comprehend the opposite side's visual/spatial field -more serious in R cortex b/c affects both sides |
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RELIGIOUS VISIONS
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-aka migrain auras
-sx: bright lights, zig-zag lines, moving counterclockwise -can have other kinds of hallucinations too dep on area of brain activated |
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NEAR DEATH EXPERIENCES
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peace and contentment-detachment from body-enter darkness-bright light-enter that light
*not all experience all stages *ketamine/oxygen starvation |
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ketamine
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dissociative anesthetic
-can induce near death experience sx -blocks glutamate receptors, esp NMDA |
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OUT OF BODY EXPERIENCES
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seizure of right angular gyrus
-interface of parietal, occipital and temporal -integrates the three to generate understanding of body's location in space |
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right angular gyrus
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in cerebral cortex, seizure here will stimulate in out of body experience
-in temporal lobe, technically -interface of parietal, occipital and temporal -integrates the three to generate understanding of body's location in space |
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DEJA VU
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caused by stimulation of temporal lobe, hippocampus, or amygdala; or temporal lobe seizure
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CT SCANNING
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*rotating X-ray source to PMTs
*shows brain damage (more watery) *computerized tomography |
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PMTs
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photo multiplier tubes
-catch deflected X-rays in CT scan |
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STANDARD ANGIOGRAPHY
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*x-ray based
*inject iodine up femoral artery into common carotid/vertebral -fairly invasive, only 2-D |
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iodine
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injected stubstance used in Standard Angiography
-shows up white |
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MRI
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*give out horizontal radio frequency pulse in vertical magnetic field = precession
*protons gradually realign (T1) and dephase (T2) and give off signals in the process = relaxation *3-D image |
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T2 signal
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horizontal magnetization decay
-protons dephasing -CSF is strongest = white |
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T1 signal
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vertical magnetization recovery
-protons realigning with vertical field -white matter is strongest = white |
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size of MRI machine's magnetic field
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3 Teslas = 30 000 Gaus
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MRA
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*inject gadolinium into blood supply
*T1 signal shows up better *3-D images of blood vessels |
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fMRI
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*uses BOLD
*able to see what areas of brain are active at any given moment in time |
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BOLD signal
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Blood Oxygen Level Detection
*deoxy Hb promotes dephasing, so in active areas, where there's more oxyHb, the T2 signal is brighter |
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PET scan
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*cyclotron shoots proton at C/N/O/F nucleus to create isotope
*isotope injected/inhaled, decays into neutron and positron *positron collides with electrion and shoots out 2 gamma rays *shows fxn, not structure |
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different PET scan methods for different isotopes
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C15: add w/ water - blood flow
F18: add w/ glucose - metabolism C11/N13: NT precursors- neuro systems |
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2PLSM
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two photon laser microscopy
GFP excited by 2 photons of infrared light, then emit these photons which can be detected and recorded -for stroke especially |
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cause of stroke
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occlusive (stenosis, embolus, thrombosis) vs. hemorrhagic
-loss of oxygen and blood = cell death (90% in 5 min) -common source: middle cerebral artery |
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occlusive stroke
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cause is blockage
-stenosis (plaque) -embolus (clot from elsewhere) -throbosis (clot from there) |
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hemorrhagic stroke
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cause is blood vessel rupture
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stroke tx
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-nothing can improve recovery
*anticoagulants/thrombolytics *a lot of research on glutamate release increase = excitotoxicity *also should look at ischemic core |
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glutamate excitotoxicity
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increased glutamate release in brain during stroke causese further excitement of pathways causing further release until neurons can no longer fire = death
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ischemic core
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centre of stroking area of brain
-cannot be recovered -experiences anoxic depolarization |
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penumbra
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area of brain surrounding ischemic core
-experiences PIDs -can be recovered??, can stop the spreading |
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PIDs
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peri-infarct depressions
-travel through penumbra |
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axons
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-perpendicular branching
-beaded -no tapering -full of vesicles |
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dendrites
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-acute angle branching
-smooth -tapers at ends |
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potassium
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[]:high inside cell, low outside
-gradient pushes out ep: -90mV -gradient pushes in -channels blocked by TEA |
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sodium
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[]: high outside, low inside
-gradient pushes in ep: +60mV -gradient pushes in, then out -channels blocked by TTX |
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chloride
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[]: high outside, low inside
-gradient pushes in ep: -40mV -gradient pushes out |
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calcium
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[]: low outside, lower inside
-gradient pushes in -channels blocked by nifedepine |
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giant squid axons
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-good for studying permeability of axonic membranes b/c of size
-study calcium and synaptic transmission |
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WHAT ARE AXONS PERMEABLE TO
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*normal resting potential = -65, increased extracell. K increases resting pot = perm to K
*AP = + number, decreased extracell. Na decreases size of AP = perm. to Na, esp in APs |
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voltage clamp technique
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-set command voltage, membrane channels respond, current counteracts the ion movement and therefore is used to measure the amt of ion current
-graph: inward = downward + vv |
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TTX
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tetrodotoxin
-blocks sodium channels |
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TEA
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tetraethylammonium
-blocks potassium channels |
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patch electrodes
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-seal end of glass rod over membrane, measure mp of one channel
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REGULAR ION CHANNELS
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-time and voltage dependent
-have intrinsic variability -have probability curve that helps determine conductance depending on membrane potential |
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persistent sodium channels
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-no time-dependent inactivation
-have constant influx to ion -9 different kinds |
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T-type calcium channels
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-voltage dependent
-time-inactivating |
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L-type calcium channels
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-voltage dependet
-non-time-inactivating |
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IF channels
aka funny channels |
hyperpolarization activated channels
-sodium or potassium -allows positive charge in if getting too negative |
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KV4.1
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-voltage dependent
-time-inactivated -inactivating after a brief outward flow |
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calcium-activated potassium channels
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as [Ca] increases, so does + outward flow
-less Ca = need more depolarizaiton to open |
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2-pore channels
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pH dependent
low pH = closed, high = open -impt for anesthetics |
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collaborating proteins
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smaller separate subunits that interact wiht alpha subunits to alter etire complex's fxn
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STEPS OF SYNAPTIC TRANSMISSION
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1. AP arrival
2. Ca channel opens 3. vesicles released 4. vesicles fuse with post-synaptic membrane = EPSP or IPSP |
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EXPERIMENTS SHOWING CALCIUM'S ROLE IN SYNAPTIC TRANSMISSION
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-more depolarization = more Ca influx
-calcium buffer -inject calcium |
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axo-axonic synapse
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-can cause presynaptic inhibition (GABAergic)
or sensitization (seritonin) |
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PRESYNAPTIC INHIBITION
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B releases GABA, Cl channels open as AP goes by in A's axon, lower amplitude of AP, less Ca channels open, less vesicles released
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QUANTAL HYPOTHESIS
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if you don't know it by now...
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deconvolution
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process of eliminating the noise at a synapse
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aplysia californica
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sea slug with gill-withdrawal reflex
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GILL WITHDRAWAL REFLEX
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draw it, please!
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LONG TERM SENSITIZATION
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result of axo-axonic synapse where the pre-synaptic terminal is induced to continue releasing NT for longer
-serotonin released-5-HT G-protein coupled receptor- ATP-->cAMP-activates pkA, into regualtory and catalytic subunits |
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regulatory subunits
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-subunit of protein kinase A
-binds with CREB in nucleus, activates expression of ubiquitin and more receptors |
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catalytic subunits
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-subunit of protein kinase A
-phosphorylates K channels, keeping membrane positive and Ca flowing in |
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ubiquitin
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detroys regulatory subunit so can't rebind with catalytic
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LONG TERM POTENTIATION
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you tell me the mechanism
-calmodulin kinase II and protein kinase C |
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PLATEAU POTENTIAL
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you tell me the mechanism
(hint: involves serotonin and post-synaptic membranes and calcium) |
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FORMATION OF AN AXON
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lamellipodia > neurites > axonal growth (1.5 days) > dendritic growth (4) > maturation (7+)
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growth cone
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-lamellipodia in veil of filipodia
-tubulin core with actin branches |
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mechanism of neuronal growth
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substrate binds to proteins > anchor actin > myosin contracts >pushes microtubules forward
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adhesion factors
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non-diffusible growth signals
*extracellular matrix: laminins, collagens, fibronectin *cell membranes: L1, NCAM, cadherins, catenins |
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chemotropic factors
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diffusible growth signals, from far away
*phosphatases, tyrosine kinases |
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FORMATION OF COMMISSURAL INTERNEURON
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DCC:netrin-1 (att)
TAG-1:NrCAM (att) Robo:Slit (rep) |
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ephrin gradient
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was on midterm, not likely to be asked again!
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SYNAPSE FORMATION
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in PNS (Ach)
in CNS (harder, maybe gamma-protocadherin) |
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gamma-protocadherin
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protein with 1000's of isoforms, might help match the right axons to the righ dendrites to make functional synapses
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PRUNING
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*chicken embroy limb buds
*neurotrophins (NGF, BDNF, NT-3, NT4/5) |
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neurotrophin receptors
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-tyrosine kinase receptors (Trk)
-p75 receptors |
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Trk A
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NGF only
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Trk B
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BDNF, NT-45, ?NT-3
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Trk C
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NT-3
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p75
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all kinds of neurotrophins
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PERIPHERAL NERVE INJURY
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1. macrophages: NGF
2. Schwann cells: myelin, NGF, BDNF, laminin 3. re-expression of GAP-43 etc crush vs transection |
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CNS INJURY PROBLEMS
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1. oligodendrocytes: no NGF/BDNF, instead NOGO, MAG, OMGP
2. macrophages: no NGF, instead cytokines 3. astrocytes: barrier plus CSPG 4. brief GAP-43 |
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CNS INJURY SOLUTIONS
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*stumps survive
*can regenerate in PNS environment and be fxnal *NOGO can be inhibited by IN-1 antibodies *neurons around it can make new branches to compensate *dendrites might turn into axons |
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scotopic
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vision in very low light
-all rods, no colour |
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mesopic
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vision in lower lights
-rods and cones |
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photopic
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-vision in bright lights
-cones (rods saturated) -higher acuity and colour etc |
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bipolar cell
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interneuron between photoreceptor and retinal ganglion cell to CNS
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receptive fields
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on/off centres
-made of retinal ganglion cells |
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horizontal cells
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cell connecting adjacent photoreceptors
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amacrine cells
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cells connecting adjacent bipolar cells
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magnocellular pathway
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retinal ganglion neuron pathway
-large cell bodies, larger receptive fields, transient response to sustained illumination, gross features of image and movement |
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parvocellular pathway
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retinal ganglion neuron pathway
-more numerous -smaller receptive fields -wavelength selective -fine detail |
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superchiasmatic nucleus
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in hypothalamus
-destination of optic tract -internal light/dark, wake/sleep cycles (circadian rhythm) |
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pretectum
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-destination of optic tract
-pupillary light reflex |
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superior colliculus
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in midbrain
-destination of optic tract -guides eye movement -receives input from posterio parietal complex, frontal eye fields and substantia nigra pars reticulata |
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lateral geniculate nucleus
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in thalamus
-destination of optic tract -main relay to visual cortex, fibres fan out from here to occipital lobe and PVC |
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calcarine sulcus
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fissure that divides primary visual cortex into lower and upper visual fields
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simple cell receptive fields
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arrangements of cells in primary cortex that receive input from on and off centre retinal ganglionic fields; represent different orientations of light in space (angles etc)
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ocular dominance groups
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for each bit of visual field, there is a gradient of where the neurons come group, and therefore which eye is the main provider of the signal
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"what" pathway
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from primary visual cortex to temporal lobe association areas
-for fine detail, colour, form |
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"where" pathway
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from primary visual cortex to parietal lobe association areas
-for motion and spatial relations |
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meissner corpuscle
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rapidly adapting receptor
-20-30 Hz sensitive -identifies kind of touch |
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pacinian corpuscule
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rapidly adapting receptor
-ID's first touch, time of touch |
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ruffini's corpuscule and merkel's disks
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slow adapting receptor
-tell us the duration of the touch |
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muscle spindle fibres
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proprioceptors (gamma motoneurons)
-wrapped around the intrafusal muscle fibres of all muslces -sense change in the length of muscle -activate when muscle lengthens |
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proprioceptors (3)
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*muscle spindle fibres
*Golgi bodies *joint receptors -fastest receptors |
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dorsal column medial lemniscal system
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somatosensory pathway
-for touch, proprioception -cross midline in caudal brainstem (gracile:lower, cuneate:upper) -first synapse: brainstem -fast conducting *ventral posterior lateral thalamus |
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anterolateral-spinal thalamic tract
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-somatosensory system
-crude touch, pain, temperature -cross midline in spinal cord -first synapse: spinal cord -slow conducting |
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trigeminal medial lemniscal system
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-somatosensory from face
-fine touch, proprioception *ventral posterior medial thalamus |
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gracile nucleus
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-in medulla
-location of lower medial somatosensory neurons |
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cuneate nucleus
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-in medulla
-location of upper lateral somatosensory neurons |
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attention centres
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in parital and frontal cortex
-lateralization exists (in right almost completely) |
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golgi bodies
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in tendons
-sense change in force of muscle by measuring stretch of tendon -tendon lenghtens = activation = inhibits contraction |
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oculomotor nerve
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CNIII
-innervates superior and inferior recti, inferior oblique and medial rectus -originates in midbrain, near vertical gaze centre |
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trochlear nerve
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CNIV
-innervates superior oblique -originates in midbrain |
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abducens nerve
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CNVI
-innervates lateral rectus -originates in pons, near horizontal gaze centre |
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step
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tonic signal that commands the eyes to hold a certain position
-height determines amplitude of saccade (distance eye travels) |
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pulse
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phasic signal that commands the eyes to move
-height=speed -duration=duration |
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horizontal gaze centre
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next to abducens in pons
aka paramedian pontine reticular formation (PPRF) |
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vertical gaze centre
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next to oculomotor centre in midbrain
aka rostral interstitial nucleus (rostral iMFL) |
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internuclear neurons
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communicate with opposite muscles in other eye so that both eyes move the same way
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excitatory burst neurons
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provide phasic signal for eye muscles to contract
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inhibitory burst neurons
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provide inhibitory signal for antagonistic muscles in eyes so eye can move
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omnipause neurons
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inhibit burst neurons in gaze centres
-silenced by trigger command from superior colliculus, which then initiates movement |
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frontal eye fields
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control production of voluntary, non-visual saccades by synapsing on superior colliculus and brain stem premotor neurons
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posterior parietal cortex
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directs voluntary visual saccades, input for superior colliculus
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ventral medial funiculus
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20-25% of spinal cord output from primary motor cortex
-synapse on medial bilateral interneurons -control posture and balance |
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ventral lateral funiciulus
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75-80% of spinal cord output form primary motor cortex
-synapse on lateral lower motor neurons and interneurons -facilitate limb movement -crosses midline in medulla |
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reticulospinal tract
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pontine and medullaru reticular formation projections down to medial bilateral interneurons
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vestibulospinal tracts
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lateral and medial vestibular nuclei projections down to medial bilateral interneurons
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colliculospinal tract
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superior colliculus projections down to medial bilateral interneurons
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rubrospinal tract
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red nucleus (input from cerebellum) projections cross midline in brainstem, lateral termination
-move entire limb, no fine motor skills |
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INPUT INTO CEREBELLAR CORTEX
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*inferior olive
*spinal cord *vestibular nucleus *pons (frontal/parietal cortex) |
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spinocerebellum
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medial part of cerebellum cortex,
input: spinal cord etc -involved in feedback control during movement |
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cerebrocerebellum
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lateral parts of cerebellum cortex
input: frontal/parietal cortex via pons -involved in initiation and planning of movement |
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deep nuclei
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below cerebellum cortex
output: thalamus > (pre)motor cortex; reticular formation |
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striatum
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caudate nucleus and putamen
input: cortex (Glu) output: globus pallidus external (GABA) and substantia nigra pars reticulata and globus pallidus internal (GABA) |
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globus pallidus external
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-indirect pathway
input: striatum (GABA) output: subthalamic nuclei (GABA) -affected by D2 |
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globus pallidus internal
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-both pathways
input: striatum (GABA) and subthalamic nuclei (Glu) output: thalamus (GABA) -with substantia nigra pars reticulata |
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substantia nigra pars compacta
|
-neither pathway
input: striatum (Glu?) output: striatum (DA) > D1 and D2 |
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substantia nigra pars reticulata
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-both pathways
input: striatum (GABA) and subthalamic nuclei (Glu) output: thalamus (GABA) -with globus pallidus internal |
|
subthalamic nuclei
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-indirect pathway
input: globus pallidus external (GABA) output: GPi and SNr (Glu) |