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Differing effects of intracortical circuits on plasticity.

J T H Teo1, C Terranova, O Swayne

  • 1Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London WC1N 3BG, UK. jteo@ion.ucl.ac.uk

Experimental Brain Research
|December 3, 2008
PubMed
Summary

Practice-dependent plasticity, an increase in motor-evoked potentials (MEP) amplitude after motor task practice, was impaired by lorazepam but not zolpidem. This suggests specific GABA(A) circuits, not GABA(A)-alpha(1) receptors, control plasticity.

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Area of Science:

  • Neuroscience
  • Motor Control
  • Neuroplasticity

Background:

  • Motor task practice enhances motor-evoked potential (MEP) amplitude, a phenomenon known as practice-dependent plasticity.
  • This plasticity is inhibited by NMDA antagonists and GABA(A) agonists like lorazepam.

Purpose of the Study:

  • To investigate whether specific GABA(A) receptor subtypes mediate the inhibitory effect of lorazepam on practice-dependent plasticity.
  • To compare the effects of a non-selective GABA(A) agonist (lorazepam) with a selective GABA(A)-alpha(1) receptor agonist (zolpidem).

Main Methods:

  • Healthy subjects practiced a ballistic motor task.
  • Transcranial magnetic stimulation (TMS) quantified MEP amplitude changes.
  • Effects of lorazepam and zolpidem on MEPs and cortical inhibitory circuits (SICI, SAI, LICI) were assessed.

Main Results:

  • Lorazepam increased short-interval intracortical inhibition (SICI) and decreased short-interval afferent inhibition (SAI).
  • Zolpidem only decreased SAI.
  • Practice-dependent plasticity was impaired by lorazepam, but not zolpidem.
  • This impairment correlated negatively with lorazepam-induced SICI changes.

Conclusions:

  • The findings suggest that intracortical circuits involved in SICI, rather than GABA(A)-alpha(1) receptor-expressing neurons, play a role in regulating practice-dependent MEP plasticity.
  • This highlights a potential mechanism for modulating motor learning and recovery.