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Nesc 2470-Dec 3rd

This document discusses Parkinson's disease and motor control. Parkinson's is caused by degeneration of neurons in the substantia nigra, leading to a lack of inhibition in the basal ganglia and symptoms like tremors and rigidity. L-Dopa treatment increases dopamine to compensate. The primary motor cortex controls movement through neurons that project to the spinal cord and receive input from other cortical and thalamic areas. The cerebellum coordinates movement through plasticity at parallel fiber synapses onto Purkinje cells, which is mediated by climbing fiber error signals, allowing motor skills to be learned.

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68 views7 pages

Nesc 2470-Dec 3rd

This document discusses Parkinson's disease and motor control. Parkinson's is caused by degeneration of neurons in the substantia nigra, leading to a lack of inhibition in the basal ganglia and symptoms like tremors and rigidity. L-Dopa treatment increases dopamine to compensate. The primary motor cortex controls movement through neurons that project to the spinal cord and receive input from other cortical and thalamic areas. The cerebellum coordinates movement through plasticity at parallel fiber synapses onto Purkinje cells, which is mediated by climbing fiber error signals, allowing motor skills to be learned.

Uploaded by

kamallery
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© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
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Nesc 2470- December 3rd 2009 12/03/2009

 Parkinsons’ Disease
 Symptoms: rigidity and tremors
 Degeneration of Substantia nigra input to putaman. Lack of inhibition of
inhibitor cells in globus pallidus. Lack of inhibition of inhibitor cells in
globus pallidus. Ventral lateral thalamic cells remain inhibited.
 L-Dopa treatment: increases dopamine release by remaining Substantia
Nigra cells.
 Increases excitatory input to inhibitory neurons of putamen
 Increases ability of frontal cortex neurons to drive inhibitory
neurons of the putamen past their activation threshold-therefore
can inhibit the inhibitors (globus pallidus)

 Primary Motor Cortex (Motor Strip)


 Elextrical Stimulation
 Contraction of small group of cells
 Ouput
 Betz cells: Pyramidal cells-to spinal cord and collaterals to brain
stem
 Two Source of input to Betz cells
 Cortical areas (e.g. accessory motor cortex)
 Thalamus (VLc- part of ventral lateral nucleus)- from cerebellum via
thalamus.

 Initiation of Movement by the Primary Motor Cortex


 The coding of Movement in M1
 Not 1 motor neuron=1 muscle
 Most cells were active no matter which direction the arm was moving

The Coding of Movement in M1 (Cont’d)


 The movement of direction encoded by collective activity of neurons.
Activity of each cell is summated and the sum of these activities
determine which way the cell will go.
 Motor Cortex: Many cells active for every movement
 Activity of each cell: Represents a single “vote”
 Direction of movement: Determined by averaging (population
vector)
 Correlation between population vector and actual direction of
movement

Neutotechnology
 Recorded spike information from monkey’s M1
 Decoded information to predict monkey's intended hand movement from
m1 spike activity.
 Used decoded m1 signal to play computer game
 monkey's could play computer game using m1

Cerebellum
 Function: Sequence of muscle contractions
 Used for balance and most motor movements
 Ataxia:
o Uncoordinated and inaccurate movements
o Caused by cerebellar lesions
 Anatomy:
 Contains more than 50% of the total neurons in CNS, about 10% of
volume
 Vermis:
o Structure at midline
o Sends output to the brainstem structures that contribute to
ventromedial pathways.

The Motor Loop through the Lateral Cerebellum


 Pontine Nuclei:
 Input relay to cerebellum
 Axons from Layer V pyramidal cells in the motor cortex and sensory
cortex form massive projections to pons.
 Corticopontocerebellar projection- projection coming from cortex to input
to cerebellum
 Lateral cerebellum projects back to motor cortex via ventral lateral
nucleus (VLc) of thalamus
 Function:
 Execution of planned, voluntary, multijoints movements

Cerebellar Plasticity
 Synaptic connections altered to learn new motor skills. Motor skills gets
encoded in cerebellum and you don’t need higher processing to carry out
movement
 Structure of the cerebellar cortex:
 Purkinje cells are large output cells with large dendritic tree that
spreads to the surface of the cerebellum. The axon goes to the
deep cellular nuclei. They are inhibitory cells.
 When climbing cell fires (wraps around the purkinje cell), the
purkinje fire.
 Purkinje cells:
o Dendrites (input) into molecular layer
o Output (axons) synapse onto deep cerebellar nuclei (output
cells of cerebellum)
o Use GABA as NT (inhibitory)
 Climbing Fibers:
o Neurons from inferior olive (medulla-muscle proprioceptors)
and then come into the cerebellum
o Axons twist around Purkinje dendrites
o Single fiber axon makes hundreds of excitatory synapses on
single Purkinje cell
o Action potential in climbing fiber activates Purkinje cell
 Mossy Fibers (input from brainstem nuclei, including those relaying
information from cerebral neocortex)
o Synapse on cerebellar granule cells
 Granule Cells:
o Numerous, in cell layer below Purkinje
o Intersect at T
o In molecular layer, axons branch to form parallel fibers
o Synapse with many different Purkinje- have a little bit of an
input into lots of Purkinje cells (to small extent)
o Use Gluatmate as NT
 Purkinje cells receive input from thousands of parallel fibers

Marr-Albus Theoyr of Motor Learning


 Can self correct if muscle movement was wrong (or too strong etc)
 Climbing fibers carry error signals that previous motor command incorrect
 Corrections made by adjusting synaptic strength of parallel fibre inputs to
Purkinje cells
 Long-Term Depression (LTD) in Cerebellar Cortex
 Stimulate Parallel fibers, EPSP in Purkinje
 Co-stimulation climbing fiber and parallel fibers
 Afterwards, stimulation of parallel fibers produce smaller EPSP.
 Synaptic Plasticity in the Cerebellar Cortex (LTD)
 Input specificity (LTD occurs only in parallel fibers synapse active
when climbing fibers active)
 Climbing fiber activation causes

Mechanism of Cerebellar LTD


 Learning
 Climbing Fiber: EPSP (Ca+ and Na+ channels open)
 Parallel Fibers- EPSP ( Na+ channels open and activation of protein
kinase C
 Both Fibers active- rise in [Ca2+], [Na+], and the activation of
protein kinase C- this results in the removal of AMPA receptors so
next time the parallel fiber fires, there will be less of a
depolarization and have less of an effect. Only fibers that are active
at the same time the climbing fiber have
 Memory
 Activation of protein kinase C n presence of higher Ca_ leads to
internalization of AMPglutamate channels
 Fewer receptors less depolarization

Motor Learning
 Results from synaptic modification
 Can be triggered by conversion of neural activity into second messenger
signal and this allows you to alter gene transmission etc
Concluding Remarks
 Example of the baseball pitcher
 Walking: Ventromedial pathways
 Ready to Pitch:
o Neocortex, ventromedial pathways
 Pitch signs and strategy:
o Sensory information engages prefrontal cortex
 Winds and throws:
o Increased basal ganglia activity (initiation)
o Accessory Motor Cortex activity  Primary motor cortex
activation
o Corticopontocerebellar pathways Cerebellum – brain stem –
spinal cord
o Cortical input to ventromedial pathways  Release of
antigravity muscles (medullary retriculospinal tract)
o Lateral pathway  engages motor neurons  action
12/03/2009

12/03/2009

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