On the intracortical activity during recruiting responses: an analysis of laminar profiles before and after topical application of GABA to the cortex.

Intracortical activity during recruiting responses (RRs) has been studied by recording laminar profiles of intracortical field potentials during repetitive stimulation, at 6 Hz, of nucleus centralis lateralis (CL) and nucleus centralis medialis (NCM) in lightly anesthetized cats, before and after topical application to the cortex of 1% GABA solution. The data obtained underwent current source density analysis (CSD) which disclosed that in the pre-GABA condition, there are two almost simultaneous sinks, one in the most superficial layer and the other in mid-cortical layers. After GABA application, a single large sink was present in mid-cortical layers. Extracellular single cortical unit activity was recorded in different animals, through a microelectrode tangentially inserted into the cortex, during repetitive stimulation of CL or NCM, both before and after GABA application. In 75% of these units there was, after GABA, a mean reduction of about 50% of firing probability while in the remaining 25% there was an increased activity. Topical application of 1% Manganese sulfate to the cortical surface appeared to completely inactivate the whole thickness of the cortex where it was applied, making evident the contribution to RRs of the potentials generated in the cortex buried in the adjacent sulci. Finally, a reciprocal facilitating effect of RRs and augmenting responses (ARs), which was studied by combined stimulation of nucleus ventralis posterolateralis (VPL) and NCM, appeared to be dependent upon an intracortical mechanism. All these data suggest that: RRs are the result of a simultaneous activation of superficial and mid-cortical layers; RRs are contaminated by a volume conducted potential arising from the cortex buried in the sulci; a superficial inhibition following the initial excitation seems to be an usual component of the response; ARs and RRs probably share a similar intracortical mechanism for incrementing the response.