L8 Flashcards
spinocerebellar tract signals cerebellum (contra/ipsi)?
ipsi
outputs from cerebellum though to?
thalamus to contralateral MC.
- control of movement
info about sensory events
- info about interneurons
1971 hypothesis: anterior spinocerebellar tract monitors ?
activity of spinal interneurons
2001 hypothesis: posterior spinocerebellar tract neurons process inputs from?
inputs from muscle afferents to get limb end-point postiion
2016 hypothesis: limb end-point derived from ?
from simple summation of proprioceptive input.
parts of cerebellum
vermis - where? sensory control?
flocculonodular lobe AKA? Used for? mediates?
spinocerebellum - where? intermediate zone does ?
cerebrocerebellum does what?
v - middle, sensory control of truncal and head movement
F AKA vestibulo-cerebellum = balance and posture
S - vermis + intermediate zones.
int = sensory control of limb movements, gait
C = sensory control of complex, adaptive hand and eye movement
inputs to cerebellum
pontine nucleus
Inferiro olive
mossy fiber
climbing fiber
pontine nucelsi
from pons . input from cerebral cortex, output of mossy fibers to cerebellum
inferior olive
brainstem, neurons synapse on IO, IO project climbing fibers to cerebellum
mossy fiber
from spinal cord & brain = provide state info
climbing fiber
from IO, strongest activity during acquisition of motor sklls/novel task.effect on purkinje cells.
all output from cerebellum =?
inhibitory
basket cell lateral inhibition
inhibit purkinje cells next to it.
mossy fiber
excite purkinje cell.
climbing fiber
elicit complex spike to produce timing cues or vary sensitivity of purkinje.
outputs from cerebellum
- purkinje via cerebellar nuclei to brain
- inhibit nuclei to which they project.
- alternat “side loop” if want to excite.
cerebellum - theories of function
- timing, sequencing
- gain control
- balance
- eye movement
- attention, cognition
- motor learning
- correct msucle activation. lesion = decomposition of movement
- control of input-output response.
- lesion = body say
- hypertremia, involuntary oscillations of eye
- cerebellum active during cogntiive tasks
- generation of new motor programs.
motor learnign in cerebellm studied
- after cerebellar damage how is motor learning affected?
- marr/albus theory
- reduced/abolished motor learning.
cerebellum maps kinematic states into motor commands. - learn from experience to map states into motor commands.
parallel fiber = delay line
climbing fiber = set gains of purkinje
evidence for climbing fibers being teacher for purkinje
mediate complex spike in purknje during motor task learning, return to baseline was learnt.
causes sensitivity of parallel fiber synapses on purkinje to be modifies
evidence for state processor role o cerebellum:
cerebellum areas process sensory signals to ID kinematic state in relatino to tasks and enviro are enlarged.
BG functions
movement initiation
context-dependent selection of motor programs
DeLong model of BG circuitry
Subs Nigra
caudate & putamen
caudate onto GP and SN (inhibitory) act on thalamus (inhibitory) act on supplementary motor.
from putamen -> inhibit GP -> inhibits STN -> excties GPi and GPe
PD
mimicked by?
rate theory based on deLong model
treatment?
decreased DA.
MPTP
- GPi & SN overactive = increased inhibition in thalamus => bradykinesia.
L-DOPA, electrical lesions
oscillatino theory of BG
abnormal in 10-25 hz = bradykinesia
abnormal burst at 60-80 hz = dyskinesia
dyskinesia
- chorea & tourrettes
- hemiballism
C&T = lesion of putamen inhibit GPe - reduce inhibition of thalamus = involuntary movement
hemiballism: withdraw inhibition of thalamus = involuntary movement
DBS
stem cells
inhibitor of dopamine breakdown
stem cells - clinical trials ceased.
rasagiline
