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457 Cards in this Set

  • Front
  • Back
who was the first person to state that neurons were the discrete elements in the CNS?
ramon y cajal
what path does current tend to follow?
the path of least resistance
what is the name for the terminal ends of the axons?
what structure is present post-synaptically that helps the neurotransmitter diffuse away quickly from its site of action?
junctional folds
what is the name for the pre-synaptic region of an axon that contains high concentrations of vesicles, neurotransmitters, and Ca channels?
active zone
what substance is made by poison dart frogs? what does it do?
curare; paralytic agent that blocks post-synaptic receptors
how fast is the response in fast synaptic transmission?
a few milliseconds
how does the Pacific electric ray catch it's prey? what type of receptors are numerous in this animal?
it has a series of modified NMJ's which are open circuits (these generate lots of current to shock their prey); nicotinic receptors
what is the name for a molecule that can be found in snake venom? what does it do?
a-bungarotoxin; it has a high affinity for the nicotinic ACh receptors in the NMJ
what type of receptor is the ACh receptor? what is the inactivation process called?
ligand gated; desensitization
what is the ACh receptor selective for?
Na, K, and Ca
the fact that there is reversal of drives at 0mV proves what?
that the ACh channel has to be permeable to more than one ion
on a voltage clamp recording, what do upward spikes represent? downward spikes?
up: K going out
down: Na going in
what is the first step of synaptic transmission? is this the rate limiting step?
vesicles fuse with the membrane and release several thousand molecules of ACh; NO, this is not rate limiting
what does the law of mass action state?
the reaction will proceed as proportional to the reactants
how many molecules of ACh have to bind to the ACh receptor?
what is a partial agonist?
a ligand that will bind to the receptor well but will not always open
what kind of agonist is ACh? what does this mean?
close to a full agonist; 99% of the receptors will simultaneously open
what kind of affinity does ACh have for it's receptor? what does this mean?
low; it will cause the receptor to open once, maybe twice, before it falls off
what are the 2 mechanisms to get rid of ACh molecules in the synapse?
diffusion and degradation
what does tetrotatoxin do? where does it come from?
blocks Na channels; pufferfish
what is the name for the number of vesicles released per stimulation?
quantal content
what is the name for the amplitude of individual responses? what is this affected by?
quantal size; decreasing the density of the receptors or making them conduct less Na
what ion must be present when you stimulate the axon?
how fast do Ca channels open compared to Na channels?
much slower
what is the rate limiting step in synaptic transmission?
the slow opening Ca channels
where are the vesicles located in the NMJ?
close to the Ca channels
what molecule is required because of the size of the NMJ?
what does inhibition of ACh-ase do?
makes the response last 4-5 times longer
what causes myasthenia gravis?
an autoimmune disorder where antibodies are directed against nicotinic ACh receptors
name a location besides the NMJ that has fast synaptic transmission. why?
auditory system; we need to hear with high fidelity
name 4 regions where synapses can occur.
directly on the soma
where do somadendritic synapses occur? what are they marked by?
occur proximally and are marked with a lot of GABA inhibition
what do axoaxonic synapses do?
allow for regulation where the NT feeds back on the presynaptic terminal and can also create cross-talk of different NTs
what ion do ligand gated ion channels in the CNS use?
what ions do ligand gated ion channels in the CNS use?
Na, K
name 3 non-selective cation ion channels.
ACh nicotinic, glutamate, or serotonergic
what do GABA and glycine receptors do?
allow Cl in
what is shunting inhibition?
when channels open that allow Cl to pour into the cell, which counteracts the movements of cations and thereby holds the membrane at RP
what are EPSPs created by?
excitatory input near dendrites
what does temporal summation depend on?
the time constant
how is glutamate neurotoxic?
it allows Ca to get into the cell via NMDA
what does most of the transmitting in the brain?
what keeps glutamate from being neurotoxic in the brain?
astrocytes that take it up out of the synapse
name 3 types of amino acid NTs and where they work.
glutamate - principle transmitter
GABA - principle transmitter
glycine - works in brain/spinal cord
what kind of cell releases glycine onto nearby motor neurons, inhibiting their function?
renshaw cells
name the 2 categories of biogenic amines and give 2 exs of each.
catecholamines - dopamine, norepinephrine
indolamines - serotonin, histamine
name 2 nucleotides that serve as NTs and give a characteristic of each.
ATP - often found stored in vesicles that contain other transmitters (such as glutamate) and is often co-released
adenosine - feeds back on the presynaptic terminals
what is the mechanism of caffiene?
it boosts signaling by inhibiting (blocking) adenosine receptors
name 2 neuropeptides and what they're involved in.
enkephalins and endorphins; involved in pain
what are 3 characteristics of the "unconventional" class of NTs?
not contained in vesicles
exhibits retrograde signaling
lipid soluble
name 2 gases that are considered NTs.
NO and CO
what is the mechanism of NO?
it activates guanylate cyclase, which increases cGMP and causes vasodilation
what does viagra do?
inhibits breakdown of cGMP, causing prolongation of the signal
what is the name of the unconventional NTs that are synthesized from arachidonic acid?
what do endocannabinoids do?
mimic the action of THC, the main substance found in marijuana
where are neuropeptides synthesized?
in the cell body
where are small peptide NTs made?
presynaptic terminal
what are the 2 types of transmitters? what is the difference?
small vesicles: 30-40 nm in diameter
dense-core vesicles: twice the size in diameter
what is the difference between dense-core vesicles and conventional (fast) transmitters?
DCV: don't dock at the active zone, tend to be further back in the terminal, need a prolonged Ca signal for fusion
where is glutamate used most?
projection neurons
name 3 places that GABA can be used.
local neurons, projection neurons, local circuit neurons (interneurons)
what is the major inhibitory NT in the brainstem and spinal cord?
what is GABA synthesis related to?
it is a side metabolic pathway related to Kreb's cycle
how is GABA made?
glutamate is converted to GABA by glutamic acid decarboxylase
how many neurons in the brain use ACh as their NT?
name 3 main areas where we find a higher density of ACh.
septal nuclei
nucleus basalis
name 3 functions of ACh.
motor behaviors
how many neurons in the brain use NE as their NT?
where is NE made in the brain?
locus ceruleus
name 5 general functions of NE.
circadian rhythms
memory formation
how many neurons in the brain use 5-HT as their NT?
what makes up the ascending projections of 5-HT? descending?
a: from the rostral raphe nuclei to nearly all the regions of the brain
d: from the caudal raphe nuclei to the spinal cord
name 3 general functions of 5-HT.
sleep/wake cycle
pain modulation
how many neurons in the brain use dopamine as their NT?
name 3 projections of the dopamanergic neurons.
substantia nigra to striatum
ventral tegmentum to: amygdale, nucleus accumbens, and prefrontal cortex
arcuate nucleus to median eminence of the hypothalamus
what does the dopamanergic projection from the substantia nigra to the striatum regulate?
largely motor movements
what does the dopamanergic projection from the ventral tegmentum to the amygdale/nucleus accumbens/prefrontal cortex regulate?
largely motivation
what does the dopamanergic projection from the arcuate nucleus to median eminence of hypothalamus regulate?
gonadatropin-releasing hormone
name 3 general functions of dopamine.
movement, motivation, and sex hormones
how is dopamine synthesized?
tyrosine --> L-dopa by tyrosine hydroxylase
L-dopa --> dopamine by dopa decarboxylase
how is NE synthesized?
dopamine --> NE by dopamine-b-hydroxylase
what types of drugs are used for depression to selectively block the reuptake of transmitters like 5-HT? what else do these drugs do?
monoamine oxidases (MAOs); also inhibit the breakdown of transmitters within cells
what are the names of the 2 classes of NT receptors?
ionitropic (aka ligand-gated)
metabotropic (aka G-protein coupled receptors)
what are the 2 types of ionitropic receptors?
excitatory nonselective (cations)
inhibitory (Cl)
what are 4 NTs that use both ionotropic and metabotropic receptors?
glutamate, ACh, GABA, 5-HT
what is one NT that uses just ionotropic receptors?
what is one NT that uses just metabotropic receptors?
dopamine and NE
what is the name for a molecule (not a NT) that activates/opens the receptor when it binds?
what type of agonist acts at the binding site and the NT that is being blocked can overcome it if in high enough concentrations?
competitive agonist
what type of agonist acts at another site on the protein to inhibit the action of the transmitter?
what type of agonist mimics ACh but doesn't produce a full effect on the receptor?
partial agonist/antagonists
what is a dose-response relationship?
you get an increasing response to a NT or agonist that will saturate
what type of receptors do benzodiazopenes and barbiturates bind to?
what is the name for the disease in which muscle ACh receptors stay open too long, leading to muscle weakness and fatigue?
congenital myasthenia
what does cholera toxin do?
stabilizes the Ga subunit, prolonging the action of that G-protein coupled receptor
what does pertussis toxin do?
destabilizes the interaction between the receptor and the heterodimer, therefore inhibiting the action of the G-protein
what does SCI refer to?
injury to the spinal cord
what does spinal elements refer to?
bony structures of the spine
what does spinal injury refer to?
injury to the spinal cord and the bony elements
name the 2 categories of spine injuries and what they are characterized on.
minor - do not cause spinal instability
major - cause spinal instability
what are the 4 main types of major spine injuries?
compression (wedge) fractures
burst fractures
what are wedge compression fractures caused by? do they result in SCIs?
axial loading/unloading with failure of the anterior column; may or may not result in SCI
what are burst fractures caused by? do they result in SCIs?
axial loading with both anterior and middle columns being compromised; typically cause SCIs
what is the critical factor in SCIs?
retropulsion elements
what is the result of fracture dislocations? do they result in SCIs?
all spinal elements of the 3 columns have burst and the vertebral body is dislocated and displaced; typically result in SCIs
what are the 2 levels of spinal cord injury and what are they characterized by?
functional incomplete: person has limited sensory and/or motor function at or below level of injury (90% of patients)
functional complete: no sensory or motor function at or below level of injury
what is the gender ratio of SCIs?
81% male, 19% female
what is the average age of SCIs? median age?
ave: 38
med: 34
what % of SCIs are sports injuries? what about diving accidents?
sports: 9%
diving: over 2/3
where is the site of injury in a typical quadriplegic? paraplegic?
quad: C4/C5
para: T12
what is the prominent etiology of SCIs in elderly females?
what tool can you use in order to determine if an SCI patient can feel at different dermatomes?
von Frey filaments
what would a C8/T1 lesion result in? what about a L1/L2/L3 lesion?
C8/T1: reduced finger abduction
L1/L2/L3: reduced hip flexion and rotation
what is the one clinically approved treatment for SCI? when do you not use this?
high-dose methylprednisone (corticosteroid); don't use for a penetrating SCI (gunshot wound)
what is the protocol for high-dose methylprednisone?
must start within 8 hrs of injury
methylprednisolone (30mg/kg) bolus administered by IV over 15 min
followed by 45 min pause
maintenance infusion of methylprednisolone (5.4 mg/kg per hr) is continued for 23 hrs
how many SCI patients have chronic neuropathic pain?
what kind of receptors may be involved in neuropathic pain in SCI patients?
nicotinic ACh receptors
what is the inheritance pattern of HD?
autosomal dominant
what is genetic anticipation?
when the age of onset tends to become younger and younger as the gene is passed down from generation to generation
what is dysarthria?
difficulty speaking
what type of mutation is present in HD?
gain of function mutation
age of onset of HD (esp juvenile) is closely correlated to what?
paternal inheritance
what are 4 things that characterize juvenile HD?
look's like Parkinsons
where is the primary pathology of HD? how do we grade the disease?
in the caudate and putamen; graded by degree of caudate atrophy
what is lost in the caudate and putamen?
medium spiny neurons (chief projection neurons of caudate/putamen)
which pathway is affected in adult onset HD? juvenile onset?
a: indirect pathway
j: both (direct and indirect)
where is the HD gene located?
short arm of chromosome 4
where is the huntingtin protein expressed?
ubiquitously in all parts of the brain and in all tissues
what is the normal CAG repeat length? normal but "mutable"? intermediate? HD?
n: <26
nbm: 27-35
i: 36-39
hd: >40
neurons of the CST are considered to be what kind of neurons?
what are the 3 areas of cortex that play a role in motor information?
primary motor cortex (pre-central gyrus)
pre-motor cortex
supplemental motor area
how many layers is the cortex (primarily)? what is this called?
6; neocortex
what parts of the brain have less than 3 layers of cells?
more ancient parts (like hippocampus)
what is the most important layer of the cortex? why?
5; it's where the main output cells are found (Betz cells)
what is the name for the main pyramidal cells that are the main outputs to the CST?
Betz cells
what is the bradmanns area # related to the main motor output from the pre-central gyrus?
what is the function of brodmanns area 4?
control of the individual movement of muscles
what is force of muscle contraction controlled by?
firing frequency
what is the brodmanns area # for the pre-motor cortex lateral?
what is the function of brodmanns area 6?
refines motor movement
what is the main output of the pre-motor cortex? what are 2 other outputs?
area 4 - main
ventral horn
reticulospinal neurons
what do connections from the pre-motor cortex to the reticulospinal neurons influence?
axial and proximal musculature
what are the 2 pathways that go to the reticulospinal neurons?
pre-motor cortex
posterior parietal cortex
what is the name for brodmanns area 6?
supplementary motor area
what is the function of the supplemental motor area?
motor planning
what is interesting about the firing of supplemental motor area neurons?
just thinking about moving will cause these neurons to fire
name 5 inputs to the primary motor cortex.
supplementary motor area
pre-motor cortex
primary sensory areas
posterior parietal
thalamic input that goes to the primary motor cortex is fed by what?
cerebellum and basal ganglia
what is a motor unit composed of?
LMN and all of the muscle cells that it innervates
what nerves are affected in Lou Gehrigs disease (ALS)?
both UMN and LMN are affected
what 2 things happen with reinnervation doesn't happen?
fibrillations and fasciculations
what is another name for fibrillations?
positive sharp waves
what do fibrillations indicate?
partial deinnervation even though there's no atrophy
what is a fasciculation?
visible little twitches in the skin that represent a motor neuron that is sick/dying but is still connected to it's motor cells
is EMG need to see a fasciculation? what about a fibrillation?
no, yes
what causes myasthenia gravis?
autoimmunity that destroys the ACh receptors and also partly the post-synaptic motor end plate
what does the large portion of botulism toxin do? small portion?
l: fools the cholinergic bouton into taking it inside (trojan horse)
s: acts as a protease that clips off one of the proteins that help the ACh vesicles dock
what are 3 things that botox can treat?
wrinkles, dystonia, muscle spasms
what does botulinum toxin type A do? type B?
A: cuts synaptobrevin (VAMP)
B: cuts SNAP-25 protein
name 4 symptoms of a cortical lesion (LCST).
contralateral body weakness
loss of fine motor control
loss of contralateral lower face
loss of contralateral half of tongue (some people)
what would result from a lesion in the pre-motor cortex alone?
slow jerky movements
difficulty in visually guided tasks
what usually happens when the pre-motor cortex is knocked out?
the primary motor cortex is also knocked out (resulting in paralysis)
what happens if you get a lesion in the supplemental motor area?
apraxia (loss of motor memory)
perseverative behavior
what is the main cause of normal pressure hydrocephalus?
waves of pressure in the CSF during sleep
what do pressure waves in the CSF result in?
3 w's:
wacky - forgetfulness
wet - bladder control problems
wobbly - apraxic gate
what is the difference between Parkinson's patients and patients with normal pressure hydrocephalus?
what can treat normal pressure hydrocephalus?
ventricular shunt
what happens with a lesion to the posterior parietal cortex? what usually occurs with this?
rare motor complaints
usually occurs with motor strip damage (paralysis)
what side of the body do posterior parietal cortex lesions occur?
symptoms occur on the left side due to a stroke on the right (dominant) side
what does the frontal eye field talk to?
contralateral PPRF
what does the PPRF talk to?
ipsi VI (LR) contra III (MR)
what is the name for the pathway that goes from the PPRF to the contralateral CN III nucleus?
medial longitudinal fasciculus
what is it called when there is a lesion in between the nuclei of III and VI?
intranuclear opthalmoplegia
if the cortex was damaged resulting in paralysis and eye deviation, what would the symptoms be?
the patient would be looking away from the paralyzed side
if the PPRF and pyramidal fascicles in the pons are damaged resulting in paralysis and eye deviation, what would the symptoms be?
patient would look towards the paralyzed side
if there was cortical activity like a seizure that produce shaking and eye deviation, what would the symptoms be?
the opposite side of the body (from the activity) would be shaking and the eyes would be deviated towards that side
if pathways are damaged near the cortex, what is the resulting symptom?
bilateral posturing
posturing is usually caused by what?
brain herniation
what is decorticate posturing? decerebrate?
flexion of arms into "O"; arm is extended with hyperpronation
what 3 cells make up what proportion of the CST?
betz cells - 40%
area 6 - 20%
posterior parietal cortex - 40%
what kind of nerves join the motor neurons of the CST?
some sensory information
what areas comprise the corticobulbar tract?
4 and 6
what is one of the major outputs as a spinal tract that serves as the UMN for the red nuclei?
corticorubral tract
where does the corticorubral tract primarily go to?
alpha motor neurons that go to the torso, head, and upper arm
where does the corticorubral tract synapse?
on interneurons of Rexed laminae V, VI, and VII of the cervical cord
where is the rubrospinal tract located?
a little ventral to the LCST in the lateral funiculus
what is the proposed function of the rubrospinal tract?
facilitate upper limb flexor motor neurons
where does the corticoreticular pathway start? where does it go through?
areas 4 and 6; goes through the posterior limb of the internal capsule
where does the corticoreticular pathway synapse? what happens to these fibers after they synapse?
neurons in the pontine and medullary reticular formation; after they synapse they make up the reticulospinal tract, which will talk to neurons in laminae VII, VIII, and IX
what are the 3 functions of the corticoreticular pathway?
goes to torso, head, and forearm alpha motor neurons
involved in setting the gamma tone
cardiovascular regulation by talking to the intermediolateral cell column
where is the corticoreticular pathway located?
near and overlapping with the spinothalamic tract. it bleeds into the ventral funiculus and some of it is in the ventral part of the lateral funiculus
what pathway modulates the motor performance via neural loops?
what are 3 things that the basal ganglia are associated with?
refining raw motor output
initiating and terminating movement
muscle tone
embryologically, where does the globus pallidus come from? what about the striatum?
gp: diencephalon
s: cortex
how and where are the caudate and putamen connected?
nucleus accumbens septi very far rostrally in the brain
what type of structure is the globus pallidus? what is it's main NT?
mainly inhibitory; NT is GABA
what structures make up the striatum?
caudate nucleus and putamen
what structures make up the corpus striatum?
caudate nucleus, putamen, and globus pallidus
what structures make up the lenticular nucleus?
putamen and globus pallidus
what structures make up the basal ganglia (formally)?
caudate nucleus, putamen, globus pallidus, amygdala, subthalamic nucleus, and substantia nigra
what is the general function of the putamen? caudate?
p: motor
c: cognition/limbic
where does the putamen receive information from? where does it send information to?
receives: motor and somatosensory cortex
projects: via the globus pallidus and thalamus to pre-motor and supplementary
where does the caudate receive information from? where does it send information to?
receives: from motor association cortex
projects: via globus pallidus and thalamus to the prefrontal cortex
what are the input nuclei of the basal ganglia?
caudate, putamen, nucleus accumbens
what are the processing nuclei of the basal ganglia?
globus pallidus (external segment), subthalamic nucleus, ventral tegmental area
what are the output nuclei of the basal ganglia?
globus pallidus (internal segment), substantia nigra pars reticulata, ventral pallidum
what is the NT of input into the basal ganglia? is this excitatory or inhibitory?
glutamate; excitatory
what is the NT of output into the basal ganglia? is this excitatory or inhibitory?
GABA; inhibitory
what are the 2 parts of the substantia nigra? what do they release?
pars compacta - dopamine
pars reticulata - functionally lumped in with the globus pallidus internal segment
what is the main output of the basal ganglia?
globus pallidus internal
where does the output of the basal ganglia go?
to the VA and VL thalamic nuclei to project back to the premotor cortex
what are the 2 pathways out of the basal ganglia?
ansa lenticularis (ventral GPi)
lenticular fasciculus (dorsal GPi)
what are the 2 major pathways within the basal ganglia? what are they responsible for?
direct - movement initiation
indirect - movement suppression
what is the primary NT of the direct pathway out of the BG?
what is the primary NT of the indirect pathway? what is the exception?
GABA; exception is the subthalamic nucleus, which is glutamate
what type of neurons are found in the substantia nigra?
median spiny (GABAergic) neurons
how many dopamine receptors are in the brain? which ones are in the striatum?
5: D1, D2, D3, D4, D5
D1 and D2 are in the striatum
what type of receptor is the D1 receptor? D2?
D1: excitatory
D2: inhibitory
what brain structure is typically involved in Huntington's disease?
what is athetosis?
slow writhing movements
what is dyskinesia?
abnormal movements
what can cause dyskinesia in Parkinson's patients?
too much treatment with Levodopa
what are ballismus? what are they usually due to?
flailing movements; usually due to stroke in the subthalamic nucleus
what are hemiballismus due to?
lesion to the STN or its projections - loss of glutamate input
what is Parkinson's due to?
degeneration of the substantia nigra pars compacta or its projections - loss of DA to both pathways
what is Huntington's due to?
lesions to striatal projections
in Parkinson's, what is the general effect of loss of DA on the direct pathway? indirect?
d: taking the brake off of GPi
i: putting your foot on the gas of GPi
what brain structure besides the substantia nigra degenerates in Parkinson's?
locus ceruleus
what mediates the deep tendon reflexes? what mediates this?
gamma motor neurons
reticulospinal tract and LCST
what is the difference between rigidity and spaticity?
spasticity is velocity dependent
what causes spasticity?
stroke takes out GABA neurons that normally inhibit gamma motor neurons. this results in too much firing, therefore increased sensitivity to stretch
the internal capsule is confluent with what?
cerebral peduncle
what are the 2 ways to get from the basal ganglia to the VA/VL nuclei of the thalamus?
go through the internal capsule via fields of forel
go under the internal capsule via ansa lenticularis
what are the 2 parts of the fields of forel?
lenticular fasciculus (H2) and thalamic fasciculus (H1)
what is the rostral most part of the sympathetic NS?
zona inserta
what part of the brain is targeted for deep brain stimulation if the patient has a tremor on the opposite side of the body? what is the caviate to this?
ventral intermedial nucleus
what part of the brain is targeted for deep brain stimulation if the patient has dystonia on the opposite side of the body?
what part of the brain is targeted for deep brain stimulation if the patient has Parkinson's?
subthalamic nucleus
name 4 symptoms of cerebellar damage.
problems with fine motor control
problems with motor programs
problems with balance
what is the name for loss or impairment of ability to execute complex coordinated movements without muscular or sensory impairment?
what is the name for an inability to coordinate voluntary muscular movements (symptomatic of some nervous disorders)?
what is another name for the superior cerebellar peduncle?
branchium conjunctiva
what are superior cerebellar fibers coming from? what are they going to?
coming from the cerebellum, heading to the contralateral thalamus and then on to the motor cortex
what is another name for the middle cerebellar peduncle? what kind of fibers does it contain?
branchium pontis; pontine fibers
what is another name for the inferior cerebellar peduncle? what is this mostly associated with?
restiform body; associated with the medulla
what fissure divides the anterior cerebellar lobe from the posterior cerebellar lobe?
primary fissure
what fissure divides the posterior cerebellar lobe from the floculonodular lobe?
the posterolateral fissure
the nodule of the cerebellum is part of what lobe?
flocculonodular lobe
the flocculonodular lobe makes up what part of the cerebellum?
the archicerebellum (the oldest part)
the paravermian cortex makes up what part of the cerebellum?
the cerebellar hemispheres make up what part of the cerebellum?
what part of the cerebellar homonculus is the archicerebellum?
vestibular, eye movements
what part of the cerebellar homonculus is the paleocerebellum?
what part of the cerebellar homonculus is the neocerebellum?
distal muscles (hands and feet)
what deep cerebellar nucleus does the neocerebellum synapse on?
what deep cerebellar nucleus does the paleocerebellum synapse on?
interposed nuclei: emboliform nucleus and globose nucleus
what deep cerebellar nucleus does the archicerebellum synapse on?
what are the names of the interposed nuclei?
emboliform nucleus and globose nucleus
fibers from what cerebellar lobe synapse directly in the vestibular nuclei?
flocculonodular lobe
what is the primary symptom of central tegmental tract damage?
palatal myoclonus
what are the 3 major cell layers of the cerebellum?
molecular cell layer
purkinje cell layer
granular cell layer
what kind of cells are in the granular layer?
granular cells
golgi cells
what are the 2 input fiber pathways into the cerebellum? are these excitatory or inhibitory?
mossy fibers and climbing fibers
both excitatory
what is the origin of the climbing fibers?
contralateral ION
what are the 2 types of cells in the molecular layer? where does each connect?
stellate cells - contact the dendritic tree or branches of the purkinje cells
basket cells - contacts the cell body or trunk of the purkinje cells
are the cells of the cerebellum excitatory or inhibitory?
all of the cells are inhibitory (GABAergic) EXCEPT FOR the granular cells (which are glutamatergic)
what is the name for the nerve terminal of a mossy fiber?
where do parallel fibers arise from?
granular cells
describe the golgi cell/granular cell loop.
granular cell excites golgi cell, which inhibits golgi cell
what is the most important monoamine in the cerebellum?
what are the 4 spinocerebellar pathways? which ones deal with arms? legs?
cuneo SCT - arms
rostral SCT - arms
dorsal SCT - legs
ventral SCT - legs
which spinocerebellar pathways has a nucleus? what is the name of that nucleus?
dorsal SCT - clark's nucleus
cuneo SCT - external cuneate nucleus
where does each spinocerebellar pathway enter the cerebellum?
cuneo SCT - ICP
rostral SCT - ICP and SCP
dorsal SCT - ICP
ventral SCT - SCP
what 2 spinocerebellar tracts are found in the lateralmost aspects of the lateral funiculus?
ventral and dorsal SCTs
what are the inputs to the ICP? outputs?
in: spinocerebellar pathways and contralateral ION
out: archicerebellar pathways efferents (en route to vestibular nuclei)
what are the inputs to the MCP? what's special about this peduncle?
in: pontine fibers
special b/c this is what causes a lesion on one side of the cerebellum to produce symptoms on the ipsilateral side of the body
what are the inputs to the SCP? outputs? where is this going?
in: rostral and ventral SCTs
out: interposed nucleus and dentate nucleus
will synapse in the VA and VL of thalamus and then head on to the motor cortex
what is the name of the reflex that is associated with the archicerebellum?
vestibular reflex or dolls eye reflex
what is another name for the archicerebellum?
what is another name for the paleocerebellum?
what is another name for the neocerebellum?
what is dysmetria?
lack of fine motor control primarily in the hands
what is dysdiadochokinesia?
inability to perform rapid alternating movements
what is a positive romberg sign?
when a person cannot stand with their eyes closed without falling over
what is the general function of the cerebellum?
it integrates all PNS information and allows execution of motor function
what structure is thought to be the site of memory storage based on increased frequency of discharge?
interpositus nucleus
what fibers are perhaps the most powerful excitatory fibers in the CNS but they don't find very often?
climbing fibers
what fibers take a lot of parallel fiber activation in order to make a purkinje fiber fire?
granular fibers
what is the sole output of the cerebellar cortex?
purkinje cell
what are 3 common causes of acute ataxia?
viral infections
hemorrhagic stroke
what are 4 common causes of chronic ataxia?
inherited degenerative disorder of the cerebellum (like SCA)
brain metastases
lesions in the flocculonodular lobe result in what symptoms?
oculomotor disturbances
lesions in the medial/vermal region result in what symptoms?
oculomotor disturbances, and problems with talking, gait, and stance
what 5 symptoms are a result from a cerebellar lesion in the intermediate and lateral zones?
intention tremor
impaired sensory motor adaptation
what is the phenotype associated with SCA 7?
hearing loss and blindness
what is the phenotype associated with SCA 6 and 10?
tremors for both
seizures for 10
what is the phenotype associated with SCA 1 and 2?
SCA 1 is what kind of inherited mutation?
does SCA 1 result in a gain or loss of function of ataxin-1?
gain of function
what are the 4 cardinal symptoms of Parkinson's?
muscle rigidity
gait instability
when does the Parkinson's tremor usually occur?
at rest
what happens in Parkinson's stage 1?
asymmetrically affecting only one side of the body
what happens in Parkinson's stage 2?
bilateral involvement
what happens in Parkinson's stage 3?
gait disturbance becomes more pronounced
what happens in Parkinson's stage 4?
patient needs help to walk
what happens in Parkinson's stage 5?
patient is in a wheelchair or bed-ridden
what are 2 non-cardinal symptoms that are common in Parkinson's?
orthostasis and autonomic symptoms
what structure degenerates in Parkinson's?
substantia nigra
what is the name for the accumulation of protein in the dopamine cells in Parkinson's?
Lewy bodies
which of the cardinal symptoms of Parkinson's can be improved by dopamine? what cannot be improved by dopamine?
muscle rigidity
postural instability and constipation cannot be improved by dopamine
what is the 5th cardinal symptom of Parkinson's?
what kind of DA receptors are found in the striatum? what kind of receptors are they?
D1: excitatory
D2: inhibitory
what is the gold standard of medicine for Parkinson's?
what does Stalevo include?
carbidopa, levodopa, and entacapone
how does levadopa work? what is a significant side effect?
it's broken down into DA
side effect: nausea and vomiting
what is a structure that degenerates in Parkinson's?
locus ceruleus
how are MDD and Parkinson's depression different?
somatic symptoms for PD depression are greater than for MDD
suicide is not as prevalent in PD depression
both have low 5-HT and NE and can be treated with Prozac
what is almost predictive of Parkinson's?
REM sleep behavior disorder
what is it called when Parkinson's patients have comorbid dementia? why?
diffuse lewy body disease
in regular PD patients lewy bodies are only present in the locus ceruleus and substantia nigra. in diffuse lewy body patients, lewy bodies are also found in the cortex
why are hallucinations associated with Parkinson's?
b/c of the excess DA
what does lack of a tremor in Parkinson's mean?
that the patient has a Parkinson's varient
what is the Parkinson's varient that is associated with problems with eye movement?
progressive supranuclear palsy
what is striatonigral degeneration?
a disease that looks like Parkinson's but does't respond to treatment
do drugs work in vascular Parkinson's? why?
no; there's no tissue for the drugs to bind to
what is an essential tremor? is it treatable with DA meds?
a tremor that doesn't occur at rest, but only occurs when the patient reaches for something
no - not DA treatable
what disease runs in families and mimics Parkinson's?
wilson's disease
what disease presents with a hummingbird sign?
progressive supranuclear palsy
what disease causes people to accumlate copper in the edge of the iris? what are these rings called?
wilson's disease
rings are kayser-fleischer rings
what are the 2 major themes of damage found in Parkinson's?
protein problems (proteosome)
what is the most famous chemical that is suspected in evironmental contributions to Parkinson's?
what is the discovered cause of familial Parkinson's?
alpha synuclein mutation
what is the oxidative stress theory of Parkinson's?
MPTP is converted to a poisonous form by monoamine oxidase type B
what normally prevents oxidation and is missing in Parkinson's patients?
does CoEnzyme Q10 have an effect on Parkinson's?
where would you inset a wire for deep brain stimulation in order to treat tremor?
ventrointermedial nucleus of the thalamus
where would you inset a wire for deep brain stimulation in order to treat Parkinson's?
subthalamic nucleus
where would you inset a wire for deep brain stimulation in order to treat dystonia?
internal part of the globus pallidus
what kind of tissue transplant seems to have a benefit for Parkinson's disease?
dopamine cells from the retina
what is the general description of ALS?
it's a progressive neurodegenerative disorder with loss of UMN and LMN function
how are glutmate levels in ALS?
increased levels, but low levels in cerebral and spinal cord tissue
what is a gene that is commonly mutated in ALS? what kind of mutation is it?
Cu/Zn SOD1 gene; gain of function
what are some UMN signs of ALS?
disruption of the CST and CBT
what are some LMN signs of ALS?
muscle weakness
what are some (more specific) features of LMN dysfunction?
weakness, atrophy, fasciculations, cramps, hyporeflexia
what are some (more specific) features of UMN dysfunction?
muscle weakness, stiffness, brisk reflexes (if weakness is too prevalent, reflexes may be hypo), poor dexterity
what are some bulbar symptoms common in ALS?
difficulty swallowing and chewing, respiratory weakness, sialorrhea
are fasciculations without weakness a cause to think about ALS?
how does Riluzole work for ALS patients?
it's a glutamate antagonist that prolongs survival by 3-6 months
what are the 4 basic attributes to a stimulus?
intensity or strength
timing or duration
what is a receptive field?
a particular area in the periphery where application of a stimulus will cause the cell to respond
how are receptors classified?
by type of stimulus or physical energy to which they are most sensitive
what are the 2 kinds of projections?
serial and parallel
what are the 4 perceptual modalities?
what kind of receptors are somatosensory receptors?
what are the 4 types of cutaneous receptors? which ones are encapsulated?
encapsulated: Pacinian, Meissner, Ruffini
unencapsulated: Merkel, free nerve endings
which cutaneous receptors are superficial? which are deep?
super: Meissners and Merkel
deep: Pacinian and Ruffini
which cutaneous receptors are rapidly adapting? slowly adapting?
rapid: Meissner and Pacinian corpuscles
slow: Merkel and Ruffini endings
what kinds of receptors detect fine tactile stimulation?
superficial: Meissners and Merkel
what are the 2 kinds of proprioceptive receptors?
muscle spindles and Golgi organ tendons
how are muscle spindles oriented? what are they sensitive to?
in parallel with the muscle, sensitive to stretching/length of the muscle
how are golgi tendon organs oriented? what are they sensitive to?
in series with the muscle, sensitive to muscle contraction
what somatosensory senses are carried by thicker axons? thinner?
thick: light/discriminatory touch
thin: pain and temperature
what pathway contains fine touch and proprioception?
dorsal column/medial lemniscal pathway
what pathway contains pain and temperature?
anterolateral system
what results from damage to one side of the spinal cord?
deficits in touch/proprioception ipsilaterally, pain contralaterally
what results from damage to one side of the medulla?
deficits for both pain and touch contralaterally
what are the 5 criteria for definition of areas of cortex?
distinctive cytoarchitecture
representative map of body surface
unique set of neural properties
unique pattern of connections
deficits result in unique deficits
what areas of the cortex does cutaneous input go to?
areas 3b and 1
what areas of the cortex does proprioceptive input go to?
areas 2 and 3a
what is a column in the cortex?
vertical collection of neurons in the cortex that all do the same thing
what cranial nerves are involved in taste?
VII, IX, X, and maybe V
what cranial nerves are involved in olfaction?
what kind of receptors are present in the olfactory system?
g-protein coupled receptors
what kind of cells are taste receptors?
modified epithelial cells
what kind of cells are smell receptors?
real neurons (unlike the other senses)
what are the components of flavor detection?
taste buds, olfactory system, and free nerve endings
what are the 3 major types of papillae on the anterior 2/3 of the tongue?
what innervates the taste buds on the anterior 2/3 of the tongue? back part of the oral cavities?
ant 2/3: chorda tympani (CN VII) and IX
post: CN X
where do the neurons from the taste buds synapse?
solitary nucleus
what nucleus is involved in reflexes of the GI tract (vomiting and swallowing)?
dorsal motor nucleus of X
is the gustatory system contralateral or ipsilateral? what about the olfactory system?
both are ipsilateral
where does the integration between taste and smell occur?
the orbitofrontal cortex
what does the labeled line theory state?
each receptor is only sensitive to submodalities
does the olfactory system synapse in the thalamus?
what kind of transduction occurs in the olfactory system?
g-protein coupled receptors
where is the initial synapse of CN I?
anterior olfactory nucleus
what are the 3 primary olfactory corticies?
piriform cortex (pre-piriform)
periamygdaloid cortex
parahippocampal gyrus
what is anosmia? what disease is this often associated with?
loss of smell; Parkinson's
where are the cell bodies of free nerve endings located? where do the projections go?
cell bodies are in the dorsal root ganglion and projections go into the CNS
what are the 3 types of nociceptors?
what modalities are carried on the alpha-delta fibers? what about the alpha-beta fibers?
AD: thermal nociception
AB: proprioception and fine touch
what kind of receptors are located on unmyelinated C fibers and result in long lasting pain?
what does substance P do?
activate mast cells leading to histamine release
what does histamine do?
sensitizes the free nerve endings, making them more responsive to other chemicals
what does arachidonic acid do?
sensitizes nociceptors
what does bradykinin do?
acts directly on alpha-delta fibers and C fibers
where do alpha-delta fibers terminate? C fibers?
AD: primarily layer 1 (marginal layer)
C: layer 2
what is the speed of conductance of AB, AD, and C fibers?
what does activation of AB fibers result in?
sharp pain
what does activation of AD fibers result in?
sharp pain
what does activation of C fibers result in?
dull burning pain
what neurotransmitters do C fibers release? what do they cause?
glutamate to signal fast synaptic transmission; secondarily release substance P which causes the release of histamine from mast cells
what kinds of temperatures do thermoreceptors respond to? what about thermal nociceptors?
TR: not extreme (20-40 C)
TN: extreme (<5 or >40 C)
what does pin prick activate?
2-point discrimination
mechanical nociceptors
what happens when nerve endings are sensitized?
a bigger response to a given stimuli occurs after the initial reaction
what does sensitization cause in terms of pain thresholds?
it decreases pain thresholds
what is hyperalgesia?
sensitization of pain receptors that decreases pain threshold
what is allodynia?
when a non-noxious stimulus becomes noxious
what part of pain does the primary somatosensory cortex deal with?
location and intensity of pain
what part of pain does the insular cortex deal with?
autonomic component
what part of pain does the anterior cingulate cortex deal with?
emotional component
what is the intensity of pain signaled by?
frequency of action potentials
what happens if you stimulate the periaqueductal gray?
you reduce pain sensation
how do enkaphalins work?
they inhibit presynatic voltage gated Ca channels to prevent release of neurotransmitters
what is the definition of pain?
unpleasant sensory and emotional experience that is associated with actual or potential tissue damage
what are pain receptors?
free nerve endings
what happens in the brain during pain?
areas of the brain receive more or less blood flow
what is nociceptive pain due to? what about neuropathic pain?
nociceptive: tissue damage
neuropathic: injury of the nervous system proper
what does nociceptive pain respond to? what about neuropathic pain?
nc: traditional analgesics
np: "adjuvant" analgesics
what are the classic signs and symptoms of nociceptive pain?
redness (rubor)
swelling (tumor)
temperature (calor)
pain (dolor)
what is the definition of sound?
sinusoidal osscillations (waves) of air compressions in an elastic medium
what is the equation for loudness?
L = 20 x log (P/Pref)
L = loudness
P = pressure
Pref = threshold of sound detection at best frequency
damage to the cochlear nucleus leads to what?
ipsilateral deafness
what frequencies does the base of the basilar membrane respond to? what about the apex of the membrane?
base: high frequencies
apex: low frequencies
what is place encoding?
frequency is encoded by the position of transduction along the basilar membrane
what kind of fluid is in the scala media? what is special about this fluid?
endolymph; extracellular solution is high in K
what kind of fluid is in the scala tympani and scala vestibuli? what does this fluid consist of?
perilymph; basically regular CSF with low levels of EC K
what are inner hair cells important for? what do they respond to?
hearing; respond to primary frequency of basilar membrane vibration
what happens when outer hair cells are lost?
loss leads to strange alterations in auditory sensitivity
which hair cells are attached to the tectorial membrane?
outer hair cells
which type of hair cells have heavier afferent innervation?
inner hair cells
what do outer hair cells do?
help recover some of the mechanical energy lost by signal dampening by the media - therefore regulating the behavior of inner hair cells and sensitivity
what does the inferior colliculus do?
helps direct your attention to sound
what is yaw?
turning head around the vertical axis like shaking the head no
what is pitch?
nodding head up and down like saying yes
what is roll?
laterally bending the head
what is the vestibulo-occular reflex?
generation of compensatory eye movements in response to head movements
what is the vestibulo-colic reflex?
maintainence of neck posture with relationship to the body despite head moving
what is the vestibulospinal reflex?
helps us maintain our posture if we start to fall over
what is the only difference between the auditory system and the vestibular system?
there are no outer hair cells in the vestibular system
what happens when the stereocilia move towards the kinocilia? what happens when they move away?
towards: depolarization
away: hyperpolarization
what are the 2 structures that detect linear acceleration?
sacculus and utricle
how are utricle hair cells partitioned? what about sacculus hair cells?
utricle: they are all pointing towards the midline
sacculus: they are all pointing away from the midline
what are the small calcium carbonate crystals in the vestibular system called?
what 2 things can activate the sacculus and utricle?
static tilt and rapid accleration without head tilt
how does your body tell the difference between head tilting and linear acceleration?
it differentiates the signal based on how long it lasts.
short signal: acceleration
long signal: tilt
how are the hair cells in the ampulla oriented?
all in the same direction
how are the horizontal SCCs oriented?
30 degrees upward of the horizontal
how are the anterior and posterior SCCs paired?
RALP: right ant left post
LARP: left ant right post
what happens to the right and left horizontal SCCs when the head is turned to the left?
the left SCC increases firing and the right SCC decreases firing
what are SCCs sensitive to? what does the firing rate of the afferent fiber correspond to?
sensitive to acceleration
firing rate corresponds to velocity
what frequencies are the vestibular system best tuned to?
what are vestibular projections in the spinal cord important for?
balance control
what are the lateral vestibulospinal tracts primarily influenced by? what are they important for?
primarily influenced by the otolith organ input
important in maintainence of posture
what are the medial vestibulospinal tract important for?
modulating head position
what are the 3 areas of cortex that vestibular signals are sent to?
face representation area of SI
area 3a
posterior parietal cortex