Mechanisms of use-dependent plasticity in the human motor cortex.
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 (an N-methyl-d-aspartate receptor blocker) and by lorazepam [a gamma-aminobutyric acid (GABA) type A receptor-positive allosteric modulator]. These results identify N-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.
Bütefisch
C M
CM
Human Cortical Physiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892-1428, USA.
Davis
B C
BC
Wise
S P
SP
Sawaki
L
L
Kopylev
L
L
Classen
J
J
Cohen
L G
LG
D003915:Dextromethorphan / Q000494:pharmacology; D005071:Evoked Potentials / Q000187:drug effects; D006801:Humans; D000077213:Lamotrigine; D017774:Long-Term Potentiation / Q000187:drug effects; D008140:Lorazepam / Q000494:pharmacology; D009044:Motor Cortex / Q000187:drug effects / Q000502:physiology*; D016202:N-Methylaspartate / Q000494:pharmacology; D014227:Triazines / Q000494:pharmacology
D014227:Triazines; D016202:N-Methylaspartate; D003915:Dextromethorphan; D008140:Lorazepam; D000077213:Lamotrigine