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Practicing movements results in improvement in performance and in plasticity of the motor cortex. To identify the underlying mechanisms, we studied use-dependent plasticity in human subjects premedicated with drugs that influence synaptic plasticity. Use-dependent plasticity was reduced substantially by dextromethorphan (anN- methyl-d -aspartate receptor blocker) and by lorazepam [a γ-aminobutyric acid (GABA) type A receptor-positive allosteric modulator]. These results identifyN -methyl-d -aspartate receptor activation and GABAergic inhibition as mechanisms operating in use-dependent plasticity in intact human motor cortex and point to similarities in the mechanisms underlying this form of plasticity and long-term potentiation.

Mechanisms of use-dependent plasticity in the human motor cortex