Hef - Cerebellum, basal ganglia, cortical function Flashcards
1
Q
cerebellum functions
A
- sequence of motor activities and corrects movements (corrective action)
- predictive action
- compare efferent motor from cerebral cortex and spinal cord info. to afferent proprioceptor info.
- planning movements - learns from mistakes
2
Q
what does cerebellum receive inputs from?
A
- efferent copy neurons from motor cortex or interneurons in spinal cord
- reafferent info. from muscle spindles, Golgi tendons, and proprioceptors
3
Q
Purkinje fibers
A
- ALWAYS inhibitory to DCN by releasing GABA
- stops the signal or prevents overshooting or oscillation
- ataxia with DCN lesion
4
Q
climbing fibers
A
- supply low # of Purkinje fibers
- communicate with DCN and higher centers
- direct action Purkinje cells, DCN, and accessory cells
- COMPLEX spikes
- comparing and building memory - TEACHERS
5
Q
mossy fibers
A
- supply high # of Purkinje cells
- communicate with granule cells –> signal to Purkinje cells
- SINGLE spikes
6
Q
other inhibitory cells of cerebellum
A
- basket, stellate, Golgi
- can participate in lateral inhibition –> sharpen signal
- always inhibitory
7
Q
vestibulocerebellum
A
predictive calculations to make anticipatory corrections to prevent one from losing balance
- direct projections to vestibular nuclei to provide sense of movements
- able to override the VOR when necessary
8
Q
spinocerebellum
A
receive info. from spinal cord - feedback control of distal limb movements
-receive copy efferent and reafferent info. then signal to DCN –> cerebral cortex and red nucleus
9
Q
cerebellum dampening functions
A
- prevent overshooting –> ataxia leads to loss of coordination, hypotonicity, and jerky movement
- prevent back and forth oscillation –> lesion lead to end tremors
- facilitate rapid alternating movements –> lesion lead to dysdiadochokinesia
10
Q
cerebrocerebellum
A
- communicate with primary, supplementary, and premotor cortex
- damage lateral zones –> lose coordination
- planning and timing of sequential movements
11
Q
Purkinje fiber affecting movement
A
fire Purkinje –> release GABA –> inhibit DCN –> inhibit motor neuron
-fire motor neuron when Purkinje stops signaling
12
Q
static vs. dynamic balance
A
static = balance and posture when not moving
dynamic = balance and posture with extreme movement
13
Q
function of the basal ganglia
A
- select important moves
- operational learning
- default –> suppress all movements (damage leads to rigidity and tremors)
- multitasking –> chunking (piece together info.)
14
Q
basal ganglia inputs
A
- input from cerebral cortex to striatum releasing GABA
- substantia nigra –> dopamine
- thalamus –> glutamate to signal cerebral cortex
- STN –> nucleus
- raphe nucleus –> serotonin
15
Q
output/intercommunication
A
- medium spiny neurons –> GABA
- interneurons –> ACh (inhibited in parkinsons)
16
Q
basal ganglia outputs
A
SNr and GPi –> always inhibitory
-signal to thalamus, pontomedullary reticular formation, and superior colliculus
17
Q
role of dopamine
A
found in substantia nigra (compact) –> Parkinson’s with damage
- tonic release –> steady state
- phasic release –> exaggerate signal –> punding
- amphetamine, cocaines, and antagonists increase dopamine levels –> movement
18
Q
hyperdirect pathway
A
use myelinated axons –> stop all actions (INHIBITORY)
- fastest response
- cerebral cortex sends a copy signal to subthalamic nucleus –> + GPi –> release GABA inhibiting thalamus –> no feedback to cortex –> shut down muscles
19
Q
direct pathway
A
- lose complex functions in parkinsons
- stimulatory and initiates movement
- dopamine acts on D1 –> tonic
- stimulate striatum –> inhibit GPi with GABA –> less GABA released from GPi –> less inhibition on thalamus –> stimulate cerebral cortex
20
Q
indirect pathway
A
net effect is inhibitory
- lesion –> excess movement
- striatum release GABA to GPe –> less GABA release to STN and GPi –> + GPi –> inhibit thalamus –> no response
21
Q
Parkinson’s disease
A
degeneration of dopamine neurons in SNc
-loss of DIRECT pathway –> no movement
22
Q
hemiballismus
A
contralateral STN lesion –> lose inhibition on thalamus bc GPi is not stimulated as much –> unusual arm movement
23
Q
Huntington disease
A
degeneration of striatum –> unusual movement
24
Q
rigidity
A
increased resistance to passive limb movement
- lead pipe –> BG lesion –> continuous rigidity throughout stretch
- cogwheel –> rigidity with phases
25
dystonia
abnormal position of limbs, face, trunk
| -result from antipsychotic drugs --> hypersensitivity when taking dopamine antagonists
26
athetosis
twisting movement of limbs, face, trunk
- chorea
- same treatment as parkinson's
27
chorea
continuous, involuntary movement that gets jerky when getting worse
- see in Huntingtons
- loss of INDIRECT pathway --> lose inhibition
28
hemiballismus
excess movement of proximal limb muscles - unilateral movement
- cause by infarct in STN
- problem with indirect pathway
29
tremors
rhythmic oscillating movements
| -resting, postural, or intention (ataxic)
30
idiopathic parkinson's disease
loss of dopamine in SNc (loss of pigmented neurons)
- deficiency of dopamine for direct path --> D1 receptors and tonic --> lead to rigidity and hypertonia
- deficiency of dopamine for indirect path --> D2 receptors and phasic --> lead to tremors
31
L-dopa
precursor for dopamine --> treat parkinson's
- on/off response
- some basal ganglia cells are cholinergic fibers --> alternate b/w ACh and dopamine when treating to prevent tolerance
32
Huntington's disease
excess movement at 1st but muscle waisting over time --> lose movement all together
- progressive atrophy of striatum
- no treatment
33
parieto-occipito-temporal association area
1. wernicke
- language and cognition on dominant side
- humor and metaphors on non-dominant side
2. angular gyrus
- metaphors, memory retrieval
- damage --> word blindness (understand something said to you but not shown to you)
34
prefrontal association area
associated with thoughts, working memory, verbal, planning, limbic system, intelligence, face recognition
-lobotomy --> loss of complex problems, planning, social problems, train of thought, mood changes
35
broca vs. wernicke area
1. broca
- motor speech on dominant
- variable tones on non-dominant
2. wernicke
- language on dominant
- humor, metaphors on non-dominant
36
aphasia
language deficit from lesions in same hemisphere
1. broca (nonfluent) - can understand, unable to speak
2. wernicke (fluent) - cannot comprehend or differentiate words, speech normal
3. conduction - cannot repeat word, but can say word if shown
37
corpus callosum
connect right and left hemispheres for bilateral functioning - crosses fibers for collaboration/coordination
38
working/immediate memory
holds info. relevant to current task - hold onto thoughts for a few sec.
- necessary for reading
- can't remember info.
39
2 types of memory loss
1. anterograde amnesia - cannot store new info.
| 2. retrograde amnesia - cannot retrieve memory
40
short term memory
- lasts for seconds or hours
- reverberating circuits
- faciliation causes memory to last longer
- tetanic stimulation: Ca2+ accumulation - more likely to fire
- posttetanic potentiation: Ca2+ level maintained
41
habituation - short term memory
loss of response due to Ca2+ not opening as well from repeated stimulation --> less Ca2+ influx --> less NT --> lose response
42
facilitation - short term memory
noxious stimulus gives you serotonin --> increase cAMP --> keeps Ca2+ open longer and closes K+ channels --> depolarize longer --> more NT release --> exaggerated response with any stimulus after that
-go back to normal when serotonin is gone
43
long term memory
- declarative - facts
- procedural - motor skill retention
- remodeling of synapses of receptors --> long lasting memory
44
long term memory mechanism - potentiation
glutamate binds to AMPA and NMDA receptors
- excess glutamate --> + AMPA --> Na+ displaces Mg2+ from NMDA exchanging for Ca2+ --> increase expression of AMPA and NMDA --> exaggerate response
- Ca2+ entry provides NO release --> more glutamate release from presynaptic neuron
- increase # of receptors and synapses
- EtOH is inhibitor of NMDA --> lose memory
45
hippocampus
memory forming center
- organizes info into long term memory
- help coordinate and consolidate memory in cerebral cortex
46
Alzheimer's disease
atrophy of the brain
- deficiency of ACh and nerve growth factor
- treatment --> prevent B-amyloid production, give NGF, or stop ACh breakdown
