Download Input sources of alpha motor neurons

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The Control of Action
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Muscles, Motor Neurons and the Spinal Cord
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Input sources of alpha motor neurons
• Alpha motor neurons receive input from sensory fibers located in the
muscles themselves
• Alpha motor neurons also receive input from the descending fibers of
the spinal cord and interneurons within the spinal segment.
• The descending fibers originate in several subcortical and cortical
structures.
• The signals can be either excitatory or inhibitory and are the basis for
voluntary movements.
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Mini-experiments: How do your hands respond to a
pressure?
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Subcortical motor structures
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Basal Ganglia
• A collection of five nuclei
• Input is restricted mainly to the two nuclei
• Output is almost exclusively by way of the internal segment of the
globus pallidus and part of the substantia nigra.
• The output is primarily ascending: axons of the globus pallidus terminate
in the thalamus, which in turn projects to motor and frontal regions of
the cerebral cortex.
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Subcortical motor structures
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Cortical motor areas
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Organization of motor areas
• Somatotopic representations of the body are found in primary and
secondary motor areas
• The motor areas form a hierarchy with multiple levels of control: the
motor control is a distributed process
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Think: Organization of a corporation
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Peripheral Control of Movement and the Role of Feedback
• The notion of hierarchical control implies that lower levels themselves can
produce movements while the higher levels can modulate the lower levels.
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The central pattern generators can produce rhythmic walking movements
without the input from the brain and the feedback from sensory neurons.
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Content of Motor Plans
Two possible ways to plan movements:
• Planning movement trajectory
• Specifying the motor commands that correspond to the target
position
Vote: which one is correct?
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Emilio Bizzi and his colleagues (1984) at the MIT showed that central
representations can be based primarily on a location code.
A simple reach experiment with deafferented monkeys showed results
that were favoring the location hypothesis.
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A follow-up study supported either predictions. The study demonstrated how
movement can be viewed as a shift from one postural state to another.
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Hierarchical representation of action
sequences
• A model developed by Donald
MacKay (1987)
• Useful in explaining the learning
of new motor patterns
Think: Organization of a corporation
(again)
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Apostolos Georgopoulos (1995)
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• Cells in motor cortex encoding movement direction
• The directional tuning is broad
• The problem of broad tuning can be solved by considering the
population vector
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John Chapin experiment (Chapin et al. 1999)
Internal Versus External Guidance of Movement
What is the contribution of secondary and association areas for motor
control?
• A dramatic demonstration was shown with TMS (Gerloff et al. 1997) on
subjects trained to produce a complex sequence of finger movement
• TMS over the motor cortex: disturbed the next response. Subjects
reported that finger suddenly seemed to jerk in the wrong direction
• TMS over SMA: the effect were delayed. The subjects reported that lost
track of their place in the sequence
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• The most significant functional aspect of the SMA is its role in coordinating
voluntary movements.
• Electrical stimulation of the supplemental (as well as premotor) cortex
requires higher currents for the elicitation of motor responses.
• The motor responses are of a more complex pattern than those elicited
from the primary motor cortex.
• SMA is responsible for internally guided movement and motor plan.
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Apraxia -- Movement disorders associated with SMA
Patients who have lesions of the SMA display apraxia.
• Ideomotor apraxia. It refers to the inability to execute a movement upon
request. An example is the failure of a patient to be able to brush his or her
hair or tie his or her shoelaces.
• Ideational apraxia. It is the inability to conceptualize the movements, and
the patient is unable to identify the sequences of movements that are
necessary for carrying out the response in question.
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The basal ganglia
• The primary function of the basal ganglia is to provide a feedback
mechanism to the cerebral cortex for the initiation and control of motor
responses
• Much of the output of the basal ganglia, which is mediated through the
thalamus, is to reduce or dampen the excitatory input to the cerebral
cortex.
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Connections of the Neostriatum with the Substantia nigra
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Modulatory role of dopamine
• D1 receptors -> increases the
excitability of MSNs and
facilitate cortico-striatal
synapses
• D2 receptors -> reduces the
excitability of MSNs and
depresses cortico-striatal
synapses
Fundamental Neuroscience. Squire et al
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Parkinson’s disease
• Parkinson’s disease is characterized by a variety of symptoms.
• The patient displays involuntary movements at rest.
• The movements are typically rhythmic tremors at approximately 3 to
6 Hz, often appearing as a “pill-rolling” tremor involving the fingers,
hands, and arm.
• Interestingly enough, the tremor disappears when the patient begins
a voluntary movement.
• The patient also displays a reduced number of spontaneous
movements (akinesia) as well as slowness of movement
(bradykinesia).
• Parkinson’s disease is now known to result from a loss of the
dopamine-containing neurons of the substantia nigra pars compacta .
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• Parkinson’s disease might also exhibit reduced amounts of
norepinephrine and serotonin elsewhere in the brain.
• Such observations indicate the heterogeneity of this disease with
respect to behavioral and neurochemical variations present in
different patients.
• Several lines of treatment therapies have been developed.
1. administration of the drug, L-3, 4-hydroxyphenylalanine (LDOPA, a precursor of dopamine)
2. Transplantation of embryonic tissue containing dopamine
neurons into the neostriatum.
3. To graft stem cells into regions where neurons have undergone
degeneration as a result of a disease process.
4. Deep-brain stimulation in STN
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Huntington’s disease (Chorea)
• Characterized by wild, uncontrolled movements of the distal musculature.
• An inherited illness with the genetic defect located on the short arm of
chromosome 4. The gene encodes a protein referred to as huntingtin.
•
One hypothesis is that the huntingtinprotein causes an induction of
apoptosis in the nucleus of the cell.
• Degeneration is extensive and involves the neostriatum, where there is
significant loss of GABA
• The later progression also involves the cerebral cortex and, in particular, the
frontal and prefrontal regions, as well as a number of other structures.
• The disease is progressive with an onset in the fifth and sixth decades of life.
• There is also a juvenile form of the disease, because of which patients usually
die before the age of 21 years.
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