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1 Division of Biological Sciences, UCSD, La Jolla, CA, USA; Zoologisches Institut, J.W. Goethe-Universitaet Frankfurt, Frankfurt am Main, Germany
2 Division of Biological Sciences, UCSD, La Jolla, CA, USA; Abteilung fuer Zellphysiologie, Max-Planck-Institut fuer Medizinische Forschung, Heidelberg, Germany
3 Division of Biological Sciences, UCSD, La Jolla, CA, USA
* To whom correspondence should be addressed. E-mail: e.foeller{at}zoology.uni-frankfurt.de.
The role of inhibition in sensory cortical map plasticity is not well understood. Here we tested whether inhibition contributes to expression of receptive field plasticity in developing rat somatosensory (S1) cortex. In normal rats, microiontophoresis of gabazine (SR 95531), a competitive 
-aminobutyric acid (GABA)-A receptor antagonist, preferentially disinhibited surround whisker responses relative to principal whisker responses, indicating that GABA-A inhibition normally acts to sharpen whisker tuning. Plasticity was induced by transiently depriving adolescent rats of all but one whisker, which causes layer 2/3 (L2/3) receptive fields to shift away from the deprived principal whisker and towards the spared surround whisker. In units with shifted receptive fields, gabazine preferentially disinhibited responses to the deprived principal whisker, unlike in controls, suggesting that GABA-A inhibition was acting to preferentially suppress these responses relative to spared whisker responses. This effect was not observed for L2/3 units that did not express receptive field plasticity, or in layer 4, where receptive field plasticity did not occur. Thus, GABA-A inhibition promoted expression of sensory map plasticity by helping to sharpen receptive fields around the spared input.
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