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159 Cards in this Set

  • Front
  • Back
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
1. lesion studies
2. monkey studies
3. fMRI imaging studies (and PET)
FXNS OF PARIETAL ASSOCATION CORTEX
*understanding sensory information
*contralateral neglect syndrome
FXNS OF TEMPORAL ASSOCIATION CORTEX
*(r)face recognition/(l)language
*recognizing complex images
FXNS OF FRONTAL ASSOCIATION CORTEX
*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
horizontal magnetization decay
-protons dephasing
-CSF is strongest = white
T1 signal
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
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
occlusive (stenosis, embolus, thrombosis) vs. hemorrhagic
-loss of oxygen and blood = cell death (90% in 5 min)
-common source: middle cerebral artery
occlusive stroke
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
peri-infarct depressions
-travel through penumbra
axons
-perpendicular branching
-beaded
-no tapering
-full of vesicles
dendrites
-acute angle branching
-smooth
-tapers at ends
potassium
[]:high inside cell, low outside
-gradient pushes out
ep: -90mV
-gradient pushes in
-channels blocked by TEA
sodium
[]: high outside, low inside
-gradient pushes in
ep: +60mV
-gradient pushes in, then out
-channels blocked by TTX
chloride
[]: high outside, low inside
-gradient pushes in
ep: -40mV
-gradient pushes out
calcium
[]: 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
*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
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
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
-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
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)