In cortical area 3b of monkeys, responses of 71 single neurons to controlled indentations of glabrous skin were recorded before and during iontophoretic application of GABA and bicuculline methiodide (BMI), a GABA receptor antagonist. Constant amplitude indentations were applied to selected sites within the receptive fields of neurons representing the glabrous skin on the digits and palm. Profiles of response magnitudes across stimulation sites were used to quantify receptive field dimensions before and during antagonism of GABAergic inhibition. During administration of BMI, the receptive fields of 26 rapidly-adapting neurons were increased by 3-4 times their original size. Response latencies were substantially longer in the region of expansion than in the original receptive field, suggesting that expansion might be mediated by intracortical connections. The expansion of RFs onto adjacent digits after blockade of GABAergic inhibition suggests that somatotopic reorganization following digit amputations may be subserved by existing excitatory connections. The responses of slowly-adapting neurons were separated into two components, a "dynamic" response corresponding to activity elicited by the initial indenting ramp and a "static" response produced by the sustained indentation. Among 8 slowly-adapting neurons tested with BMI, the receptive fields of the dynamic response component increased to an extent that was similar to the change produced in rapidly-adapting neurons. By contrast, the static response component was rarely altered by BMI. Comparison of the responses to administration of GABA revealed that only 12 of 27 slowly-adapting neurons were inhibited in a dose-dependent manner, whereas 37 of 44 rapidly-adapting neurons exhibited significant reduction of responses in the presence of GABA. Hypotheses are proposed to explain the differential effect of BMI and GABA on slowly- and rapidly-adapting cortical neurons.
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