Spinal Cord Injury Clinical Trial
Official title:
Mechanisms of Plasticity in the Human Motor System
The purpose of this study is to investigate the physiology associated with plasticity of the
motor system. Plasticity refers to the process by which neighboring brain cells assume the
responsibilities of damaged or diseased brain cells.
The mechanisms behind this process are unknown. However, researchers have several theories
about how plastic changes take place. Possible explanations include the growth of new
connections between brain cells and the use of previously unused connections.
Researchers plan to use transcranial magnetic stimulation and drug intervention in order to
determine the mechanisms responsible for specific types of plasticity.
Previous studies have shown that certain drugs can affect the mechanisms involved in these
changes. By using one drug at a time, researchers plan to evaluate the role of each of
several different mechanisms in brain reorganization.
The purpose of this study is to investigate the physiology associated with plasticity of the
motor system seen in a number of different circumstances. Techniques used will involve the
combination of transcranial magnetic stimulation (TMS) and pharmacologic interventions. We
propose to use drugs judged to be safe, that either potentiate GABA related intracortical
inhibition, change presynaptic release of excitatory aminoacids like glutamate, or decrease
the activity of the NMDA receptors (mostly antiepileptic drugs). If plastic changes
expressed as larger motor maps or motor evoked potentials (MEP) to TMS are secondary to
intracortical disinhibition, administration of a drug that potentiates intracortical
inhibition may result in decreased plasticity and smaller motor maps or MEP. This finding
would then identify intracortical disinhibition as the mechanism responsible for this type
of plasticity. Similarly, if plastic changes decrease with a drug that inhibits release of
excitatory aminoacids, or that antagonize the action of NMDA receptors, the mechanism
underlying plasticity is likely to be mediated by modulation in the release of excitatory
aminoacids or activity in NMDA-receptors.
Results from this study will then provide information about the relative involvement of
intracortical disinhibition, modulation in the release of excitatory aminoacids, and role of
NMDA receptors in different settings of human plasticity.
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N/A
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