Hef - Cerebellum, basal ganglia, cortical function Flashcards
cerebellum functions
- 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
what does cerebellum receive inputs from?
- efferent copy neurons from motor cortex or interneurons in spinal cord
- reafferent info. from muscle spindles, Golgi tendons, and proprioceptors
Purkinje fibers
- ALWAYS inhibitory to DCN by releasing GABA
- stops the signal or prevents overshooting or oscillation
- ataxia with DCN lesion
climbing fibers
- 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
mossy fibers
- supply high # of Purkinje cells
- communicate with granule cells –> signal to Purkinje cells
- SINGLE spikes
other inhibitory cells of cerebellum
- basket, stellate, Golgi
- can participate in lateral inhibition –> sharpen signal
- always inhibitory
vestibulocerebellum
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
spinocerebellum
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
cerebellum dampening functions
- 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
cerebrocerebellum
- communicate with primary, supplementary, and premotor cortex
- damage lateral zones –> lose coordination
- planning and timing of sequential movements
Purkinje fiber affecting movement
fire Purkinje –> release GABA –> inhibit DCN –> inhibit motor neuron
-fire motor neuron when Purkinje stops signaling
static vs. dynamic balance
static = balance and posture when not moving
dynamic = balance and posture with extreme movement
function of the basal ganglia
- select important moves
- operational learning
- default –> suppress all movements (damage leads to rigidity and tremors)
- multitasking –> chunking (piece together info.)
basal ganglia inputs
- input from cerebral cortex to striatum releasing GABA
- substantia nigra –> dopamine
- thalamus –> glutamate to signal cerebral cortex
- STN –> nucleus
- raphe nucleus –> serotonin
output/intercommunication
- medium spiny neurons –> GABA
- interneurons –> ACh (inhibited in parkinsons)
basal ganglia outputs
SNr and GPi –> always inhibitory
-signal to thalamus, pontomedullary reticular formation, and superior colliculus
role of dopamine
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
hyperdirect pathway
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
direct pathway
- 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
indirect pathway
net effect is inhibitory
- lesion –> excess movement
- striatum release GABA to GPe –> less GABA release to STN and GPi –> + GPi –> inhibit thalamus –> no response
Parkinson’s disease
degeneration of dopamine neurons in SNc
-loss of DIRECT pathway –> no movement
hemiballismus
contralateral STN lesion –> lose inhibition on thalamus bc GPi is not stimulated as much –> unusual arm movement
Huntington disease
degeneration of striatum –> unusual movement
rigidity
increased resistance to passive limb movement
- lead pipe –> BG lesion –> continuous rigidity throughout stretch
- cogwheel –> rigidity with phases
dystonia
abnormal position of limbs, face, trunk
-result from antipsychotic drugs –> hypersensitivity when taking dopamine antagonists
athetosis
twisting movement of limbs, face, trunk
- chorea
- same treatment as parkinson’s
chorea
continuous, involuntary movement that gets jerky when getting worse
- see in Huntingtons
- loss of INDIRECT pathway –> lose inhibition
hemiballismus
excess movement of proximal limb muscles - unilateral movement
- cause by infarct in STN
- problem with indirect pathway
tremors
rhythmic oscillating movements
-resting, postural, or intention (ataxic)
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
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
Huntington’s disease
excess movement at 1st but muscle waisting over time –> lose movement all together
- progressive atrophy of striatum
- no treatment
parieto-occipito-temporal association area
- wernicke
- language and cognition on dominant side
- humor and metaphors on non-dominant side - angular gyrus
- metaphors, memory retrieval
- damage –> word blindness (understand something said to you but not shown to you)
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
broca vs. wernicke area
- broca
- motor speech on dominant
- variable tones on non-dominant - wernicke
- language on dominant
- humor, metaphors on non-dominant
aphasia
language deficit from lesions in same hemisphere
- broca (nonfluent) - can understand, unable to speak
- wernicke (fluent) - cannot comprehend or differentiate words, speech normal
- conduction - cannot repeat word, but can say word if shown
corpus callosum
connect right and left hemispheres for bilateral functioning - crosses fibers for collaboration/coordination
working/immediate memory
holds info. relevant to current task - hold onto thoughts for a few sec.
- necessary for reading
- can’t remember info.
2 types of memory loss
- anterograde amnesia - cannot store new info.
2. retrograde amnesia - cannot retrieve memory
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
habituation - short term memory
loss of response due to Ca2+ not opening as well from repeated stimulation –> less Ca2+ influx –> less NT –> lose response
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
long term memory
- declarative - facts
- procedural - motor skill retention
- remodeling of synapses of receptors –> long lasting memory
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
hippocampus
memory forming center
- organizes info into long term memory
- help coordinate and consolidate memory in cerebral cortex
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
