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J Neurophysiol (May 1, 2003). 10.1152/jn.00900.2002
Submitted on Submitted 8 October 2002; accepted in final form 18 January
2003
TRANSLATIONAL PHYSIOLOGY
1Human Cortical Physiology Laboratory, Department of Neurology, University of Rostock, D-18147 Rostock, Germany; 2Human Cortical Physiology Section, National Institute of Neurological Disorders and Stroke, Medical Neurology Branch, National Institutes of Health, Bethesda, Maryland; and 3Human Cortical Physiology and Motor Control Laboratory, Department of Neurology, University of Wuerzburg, D-97080 Wuerzburg, Germany
Wolters, Alexander,
Friedhelm Sandbrink,
Antje Schlottmann,
Erwin Kunesch,
Katja Stefan,
Leonardo G. Cohen,
Reiner Benecke, and
Joseph Classen.
A Temporally Asymmetric Hebbian Rule Governing Plasticity in the
Human Motor Cortex. J. Neurophysiol. 89: 2339-2345, 2003. Synaptic plasticity is
conspicuously dependent on the temporal order of the pre- and
postsynaptic activity. Human motor cortical excitability can be
increased by a paired associative stimulation (PAS) protocol. Here we
show that it can also be decreased by minimally changing the interval
between the two associative stimuli. Corticomotor excitability of the
abductor pollicis brevis (APB) representation was tested before and
after repetitively pairing of single right median nerve simulation with
single pulse transcranial magnetic stimulation (TMS) delivered over the
optimal site for activation of the contralateral APB. Following PAS,
depression of TMS-evoked motor-evoked potentials (MEPs) was induced
only when the median nerve stimulation preceded the TMS pulse by 10 ms,
while enhancement of cortical excitability was induced using an
interstimulus interval of 25 ms, suggesting an important role of the
sequence of cortical events triggered by the two stimulation modalities. Experiments using F-wave studies and electrical brain stem
stimulation indicated that the site of the plastic changes underlying
the decrease of MEP amplitudes following PAS (10 ms) was within the
motor cortex. MEP amplitudes remained depressed for approximately 90 min. The decrease of MEP amplitudes was blocked when PAS(10 ms) was
performed under the influence of dextromethorphan, an
N-methyl-D-aspartate-receptor antagonist, or
nimodipine, an L-type voltage-gated calcium-channel antagonist. The
physiological profile of the depression of human motor cortical
excitability following PAS(10 ms) suggests long-term depression of
synaptic efficacy to be involved. Together with earlier findings, this study suggests that strict temporal Hebbian rules govern the induction of long-term potentiation/long-term depression-like phenomena in vivo in the human primary motor cortex.
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