Corticostriatal transmission has an important function in the regulation of the neuronal activity of the basal ganglia. The firing activity of corticostriatal neurones excites striatal cells via the release of glutamate. Presynaptic receptors that are located on corticostriatal terminals and that regulate the release of glutamate in the striatum have been postulated for dopamine and glutamate. Activation of these receptors may exert a negative feed-back on the striatal release of glutamate. High-frequency activation of corticostriatal fibres causes either long-term depression or long-term potentiation of excitatory transmission depending on the subclass of glutamate receptor that is activated. These forms of synaptic plasticity could be involved in motor learning. Alterations in striatal synaptic plasticity might be implicated in Parkinson's disease and Huntington's disease.
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