LISC 322
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- paleocortex
- primary olfactory cortex, a layer of primitive cortex
- archicortex
- hippocampal formation layer of primitive cortex
- neocortex
- third layer of primitive cortex, contains 6 layers of its own
- layers III and V of neocortex
- output neurons that contribute to axons of underlying white matter
- layers II and IV of neocortex
- contain interneurons, dentrites from III and V, and myelinated input from thalamus and other cortical areas
- motor association areas
-
1. premotor area
2. frontal eye fields
3. motor speech area of Broca
4. supplementary motor area - 4 distinctly human traits
-
1. complex language
2. precision movements of the hands and eyes
3. incredible memory storage
4. the power of forethought - 4 pieces of indirect evidence that neocortex is involved with higher thought processing
-
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 - gestational time of neuronal development
-
1 mo- no brain
2 mos- 1 cm of brain
4 mos- neocortex appears
7 mos- very developed, i guess - EPILEPSY
-
*periodic and unpredictable seizures
*hyderexcitable and hypersynchronous brain
*epileptic focus = starting pt
*brain slice experiments - ALZHEIMER'S
-
*form of dementia
*neocortex shrivelled
*cholinergic neurons from basal forebrain to neocortex/hippocampus die
*neurofibrillary tangles and amyloid plaques - epileptic focus
- starting point of seizure that spreads to otehr areas
- neurofibrillary tangles
-
shrunken neural processes get tangled
-Alzheimer's - amyloid plaques
-
junk outside tangles = detrimental to brian fxn
-Alzheimer's - 3 ways to study fxn of association cortex
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1. lesion studies
2. monkey studies
3. fMRI imaging studies (and PET) - FXNS OF PARIETAL ASSOCATION CORTEX
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*understanding sensory information
*contralateral neglect syndrome - FXNS OF TEMPORAL ASSOCIATION CORTEX
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*(r)face recognition/(l)language
*recognizing complex images - FXNS OF FRONTAL ASSOCIATION CORTEX
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*behaviour
*social skills
*planning - contralateral neglect syndrome
-
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 - RELIGIOUS VISIONS
-
-aka migrain auras
-sx: bright lights, zig-zag lines, moving counterclockwise
-can have other kinds of hallucinations too dep on area of brain activated - NEAR DEATH EXPERIENCES
-
peace and contentment-detachment from body-enter darkness-bright light-enter that light
*not all experience all stages
*ketamine/oxygen starvation - ketamine
-
dissociative anesthetic
-can induce near death experience sx
-blocks glutamate receptors, esp NMDA - OUT OF BODY EXPERIENCES
-
seizure of right angular gyrus
-interface of parietal, occipital and temporal
-integrates the three to generate understanding of body's location in space - right angular gyrus
-
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 - DEJA VU
- caused by stimulation of temporal lobe, hippocampus, or amygdala; or temporal lobe seizure
- CT SCANNING
-
*rotating X-ray source to PMTs
*shows brain damage (more watery)
*computerized tomography - PMTs
-
photo multiplier tubes
-catch deflected X-rays in CT scan - STANDARD ANGIOGRAPHY
-
*x-ray based
*inject iodine up femoral artery into common carotid/vertebral
-fairly invasive, only 2-D - iodine
-
injected stubstance used in Standard Angiography
-shows up white - MRI
-
*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 - T2 signal
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horizontal magnetization decay
-protons dephasing
-CSF is strongest = white - T1 signal
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vertical magnetization recovery
-protons realigning with vertical field
-white matter is strongest = white - size of MRI machine's magnetic field
- 3 Teslas = 30 000 Gaus
- MRA
-
*inject gadolinium into blood supply
*T1 signal shows up better
*3-D images of blood vessels - fMRI
-
*uses BOLD
*able to see what areas of brain are active at any given moment in time - 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 - PET scan
-
*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 - different PET scan methods for different isotopes
-
C15: add w/ water - blood flow
F18: add w/ glucose - metabolism
C11/N13: NT precursors- neuro systems - 2PLSM
-
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 - 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 - occlusive stroke
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cause is blockage
-stenosis (plaque)
-embolus (clot from elsewhere)
-throbosis (clot from there) - hemorrhagic stroke
- cause is blood vessel rupture
- stroke tx
-
-nothing can improve recovery
*anticoagulants/thrombolytics
*a lot of research on glutamate release increase = excitotoxicity
*also should look at ischemic core - glutamate excitotoxicity
- increased glutamate release in brain during stroke causese further excitement of pathways causing further release until neurons can no longer fire = death
- ischemic core
-
centre of stroking area of brain
-cannot be recovered
-experiences anoxic depolarization - penumbra
-
area of brain surrounding ischemic core
-experiences PIDs
-can be recovered??, can stop the spreading - PIDs
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peri-infarct depressions
-travel through penumbra - axons
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-perpendicular branching
-beaded
-no tapering
-full of vesicles - dendrites
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-acute angle branching
-smooth
-tapers at ends - potassium
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[]:high inside cell, low outside
-gradient pushes out
ep: -90mV
-gradient pushes in
-channels blocked by TEA - sodium
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[]: high outside, low inside
-gradient pushes in
ep: +60mV
-gradient pushes in, then out
-channels blocked by TTX - chloride
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[]: high outside, low inside
-gradient pushes in
ep: -40mV
-gradient pushes out - calcium
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[]: low outside, lower inside
-gradient pushes in
-channels blocked by nifedepine - giant squid axons
-
-good for studying permeability of axonic membranes b/c of size
-study calcium and synaptic transmission - 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 - voltage clamp technique
-
-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 - TTX
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tetrodotoxin
-blocks sodium channels - TEA
-
tetraethylammonium
-blocks potassium channels - patch electrodes
- -seal end of glass rod over membrane, measure mp of one channel
- REGULAR ION CHANNELS
-
-time and voltage dependent
-have intrinsic variability
-have probability curve that helps determine conductance depending on membrane potential - persistent sodium channels
-
-no time-dependent inactivation
-have constant influx to ion
-9 different kinds - T-type calcium channels
-
-voltage dependent
-time-inactivating - L-type calcium channels
-
-voltage dependet
-non-time-inactivating -
IF channels
aka funny channels -
hyperpolarization activated channels
-sodium or potassium
-allows positive charge in if getting too negative - KV4.1
-
-voltage dependent
-time-inactivated
-inactivating after a brief outward flow - calcium-activated potassium channels
-
as [Ca] increases, so does + outward flow
-less Ca = need more depolarizaiton to open - 2-pore channels
-
pH dependent
low pH = closed, high = open
-impt for anesthetics - collaborating proteins
- smaller separate subunits that interact wiht alpha subunits to alter etire complex's fxn
- 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 - EXPERIMENTS SHOWING CALCIUM'S ROLE IN SYNAPTIC TRANSMISSION
-
-more depolarization = more Ca influx
-calcium buffer
-inject calcium - axo-axonic synapse
-
-can cause presynaptic inhibition (GABAergic)
or sensitization (seritonin) - PRESYNAPTIC INHIBITION
- 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
- QUANTAL HYPOTHESIS
- if you don't know it by now...
- deconvolution
- process of eliminating the noise at a synapse
- aplysia californica
- sea slug with gill-withdrawal reflex
- GILL WITHDRAWAL REFLEX
- draw it, please!
- LONG TERM SENSITIZATION
-
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 - regulatory subunits
-
-subunit of protein kinase A
-binds with CREB in nucleus, activates expression of ubiquitin and more receptors - catalytic subunits
-
-subunit of protein kinase A
-phosphorylates K channels, keeping membrane positive and Ca flowing in - ubiquitin
- detroys regulatory subunit so can't rebind with catalytic
- LONG TERM POTENTIATION
-
you tell me the mechanism
-calmodulin kinase II and protein kinase C - PLATEAU POTENTIAL
-
you tell me the mechanism
(hint: involves serotonin and post-synaptic membranes and calcium) - FORMATION OF AN AXON
- lamellipodia > neurites > axonal growth (1.5 days) > dendritic growth (4) > maturation (7+)
- growth cone
-
-lamellipodia in veil of filipodia
-tubulin core with actin branches - mechanism of neuronal growth
- substrate binds to proteins > anchor actin > myosin contracts >pushes microtubules forward
- adhesion factors
-
non-diffusible growth signals
*extracellular matrix: laminins, collagens, fibronectin
*cell membranes: L1, NCAM, cadherins, catenins - chemotropic factors
-
diffusible growth signals, from far away
*phosphatases, tyrosine kinases - FORMATION OF COMMISSURAL INTERNEURON
-
DCC:netrin-1 (att)
TAG-1:NrCAM (att)
Robo:Slit (rep) - ephrin gradient
- was on midterm, not likely to be asked again!
- SYNAPSE FORMATION
-
in PNS (Ach)
in CNS (harder, maybe gamma-protocadherin) - gamma-protocadherin
- protein with 1000's of isoforms, might help match the right axons to the righ dendrites to make functional synapses
- PRUNING
-
*chicken embroy limb buds
*neurotrophins (NGF, BDNF, NT-3, NT4/5) - neurotrophin receptors
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-tyrosine kinase receptors (Trk)
-p75 receptors - Trk A
- NGF only
- Trk B
- BDNF, NT-45, ?NT-3
- Trk C
- NT-3
- p75
- all kinds of neurotrophins
- PERIPHERAL NERVE INJURY
-
1. macrophages: NGF
2. Schwann cells: myelin, NGF, BDNF, laminin
3. re-expression of GAP-43 etc
crush vs transection - 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 - CNS INJURY SOLUTIONS
-
*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 - scotopic
-
vision in very low light
-all rods, no colour - mesopic
-
vision in lower lights
-rods and cones - photopic
-
-vision in bright lights
-cones (rods saturated)
-higher acuity and colour etc - bipolar cell
- interneuron between photoreceptor and retinal ganglion cell to CNS
- receptive fields
-
on/off centres
-made of retinal ganglion cells - horizontal cells
- cell connecting adjacent photoreceptors
- amacrine cells
- cells connecting adjacent bipolar cells
- magnocellular pathway
-
retinal ganglion neuron pathway
-large cell bodies, larger receptive fields, transient response to sustained illumination, gross features of image and movement - parvocellular pathway
-
retinal ganglion neuron pathway
-more numerous
-smaller receptive fields
-wavelength selective
-fine detail - superchiasmatic nucleus
-
in hypothalamus
-destination of optic tract
-internal light/dark, wake/sleep cycles (circadian rhythm) - pretectum
-
-destination of optic tract
-pupillary light reflex - superior colliculus
-
in midbrain
-destination of optic tract
-guides eye movement
-receives input from posterio parietal complex, frontal eye fields and substantia nigra pars reticulata - lateral geniculate nucleus
-
in thalamus
-destination of optic tract
-main relay to visual cortex, fibres fan out from here to occipital lobe and PVC - calcarine sulcus
- fissure that divides primary visual cortex into lower and upper visual fields
- simple cell receptive fields
- 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)
- ocular dominance groups
- 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
- "what" pathway
-
from primary visual cortex to temporal lobe association areas
-for fine detail, colour, form - "where" pathway
-
from primary visual cortex to parietal lobe association areas
-for motion and spatial relations - meissner corpuscle
-
rapidly adapting receptor
-20-30 Hz sensitive
-identifies kind of touch - pacinian corpuscule
-
rapidly adapting receptor
-ID's first touch, time of touch - ruffini's corpuscule and merkel's disks
-
slow adapting receptor
-tell us the duration of the touch - muscle spindle fibres
-
proprioceptors (gamma motoneurons)
-wrapped around the intrafusal muscle fibres of all muslces
-sense change in the length of muscle
-activate when muscle lengthens - proprioceptors (3)
-
*muscle spindle fibres
*Golgi bodies
*joint receptors
-fastest receptors - dorsal column medial lemniscal system
-
somatosensory pathway
-for touch, proprioception
-cross midline in caudal brainstem (gracile:lower, cuneate:upper)
-first synapse: brainstem
-fast conducting
*ventral posterior lateral thalamus - anterolateral-spinal thalamic tract
-
-somatosensory system
-crude touch, pain, temperature
-cross midline in spinal cord
-first synapse: spinal cord
-slow conducting - trigeminal medial lemniscal system
-
-somatosensory from face
-fine touch, proprioception
*ventral posterior medial thalamus - gracile nucleus
-
-in medulla
-location of lower medial somatosensory neurons - cuneate nucleus
-
-in medulla
-location of upper lateral somatosensory neurons - attention centres
-
in parital and frontal cortex
-lateralization exists (in right almost completely) - golgi bodies
-
in tendons
-sense change in force of muscle by measuring stretch of tendon
-tendon lenghtens = activation = inhibits contraction - oculomotor nerve
-
CNIII
-innervates superior and inferior recti, inferior oblique and medial rectus
-originates in midbrain, near vertical gaze centre - trochlear nerve
-
CNIV
-innervates superior oblique
-originates in midbrain - abducens nerve
-
CNVI
-innervates lateral rectus
-originates in pons, near horizontal gaze centre - step
-
tonic signal that commands the eyes to hold a certain position
-height determines amplitude of saccade (distance eye travels) - pulse
-
phasic signal that commands the eyes to move
-height=speed
-duration=duration - horizontal gaze centre
-
next to abducens in pons
aka paramedian pontine reticular formation (PPRF) - vertical gaze centre
-
next to oculomotor centre in midbrain
aka rostral interstitial nucleus (rostral iMFL) - internuclear neurons
- communicate with opposite muscles in other eye so that both eyes move the same way
- excitatory burst neurons
- provide phasic signal for eye muscles to contract
- inhibitory burst neurons
- provide inhibitory signal for antagonistic muscles in eyes so eye can move
- omnipause neurons
-
inhibit burst neurons in gaze centres
-silenced by trigger command from superior colliculus, which then initiates movement - frontal eye fields
- control production of voluntary, non-visual saccades by synapsing on superior colliculus and brain stem premotor neurons
- posterior parietal cortex
- directs voluntary visual saccades, input for superior colliculus
- ventral medial funiculus
-
20-25% of spinal cord output from primary motor cortex
-synapse on medial bilateral interneurons
-control posture and balance - ventral lateral funiciulus
-
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 - reticulospinal tract
- pontine and medullaru reticular formation projections down to medial bilateral interneurons
- vestibulospinal tracts
- lateral and medial vestibular nuclei projections down to medial bilateral interneurons
- colliculospinal tract
- superior colliculus projections down to medial bilateral interneurons
- rubrospinal tract
-
red nucleus (input from cerebellum) projections cross midline in brainstem, lateral termination
-move entire limb, no fine motor skills - INPUT INTO CEREBELLAR CORTEX
-
*inferior olive
*spinal cord
*vestibular nucleus
*pons (frontal/parietal cortex) - spinocerebellum
-
medial part of cerebellum cortex,
input: spinal cord etc
-involved in feedback control during movement - cerebrocerebellum
-
lateral parts of cerebellum cortex
input: frontal/parietal cortex via pons
-involved in initiation and planning of movement - deep nuclei
-
below cerebellum cortex
output: thalamus > (pre)motor cortex; reticular formation - striatum
-
caudate nucleus and putamen
input: cortex (Glu)
output: globus pallidus external (GABA) and substantia nigra pars reticulata and globus pallidus internal (GABA) - globus pallidus external
-
-indirect pathway
input: striatum (GABA)
output: subthalamic nuclei (GABA)
-affected by D2 - globus pallidus internal
-
-both pathways
input: striatum (GABA) and subthalamic nuclei (Glu)
output: thalamus (GABA)
-with substantia nigra pars reticulata - substantia nigra pars compacta
-
-neither pathway
input: striatum (Glu?)
output: striatum (DA) > D1 and D2 - substantia nigra pars reticulata
-
-both pathways
input: striatum (GABA) and subthalamic nuclei (Glu)
output: thalamus (GABA)
-with globus pallidus internal - subthalamic nuclei
-
-indirect pathway
input: globus pallidus external (GABA)
output: GPi and SNr (Glu)