1. A 16-channel electrode array was used to record simultaneously extracellular laminar field potentials evoked by displacement of contralateral vibrissa from vibrissa/barrel cortex in five rats. Current source-density (CSD) analysis combined with principal component analysis (PCA) was used to determine the time course of laminar-specific transmembrane currents during the evoked response. 2. The potential complex consisted of biphasic fast components followed by long-lasting slow waves. It began with activity in supragranular cells consisting of a source in layers I-II and a sink in layers IV-V; this was followed by activation of the infragranular cells with a paired sink and source in layers I-IV and V-VI, respectively. The slow-wave sequences also began in the supragranular cells followed by infragranular neurons. 3. We propose that the fast components reflect sequential intralaminar depolarization processes, and the slow waves, hyper- or repolarization processes. These results suggest that a basic neuronal circuit, consisting of sequential activation of the supragranular and then the infragranular pyramidal cells, gives rise to the field potentials evoked by physiological stimulation. This is consistent with our previous studies of direct cortical responses (DCR) and pathological discharges of the penicillin focus.

No abstract

1. A 8 X 8-channel microelectrode array was used to map epicortical field potentials evoked by bilaterally presented click stimuli from a 8 X 8-mm2 area in the right parietotemporal neocortex of four rats. In two rats, a 16-channel microelectrode array was also inserted into primary auditory cortex to record the laminar profile of auditory evoked potentials (AEP). 2. The epicortical responses began with a positive-negative fast wave followed by a positive-negative slow wave, similar to the previously reported P1, N1, P2, N2 complex. Topographical distributions of the potentials at the peak of each of these waves were distinct, suggesting that they were produced by separate but overlapping populations of cells. 3. Laminar recording revealed the asynchronous participation of supragranular and infragranular pyramidal cells in the generation of the evoked-response complex. The surface-recorded P1 was primarily produced by supragranular cells and the N1, by infragranular cells. The P2 and N2 were produced by temporally overlapping contributions from both cell groups. 4. We conclude that middle-latency components of the AEP complex are produced by both sequential and parallel activation of subpopulations of pyramidal cells in primary auditory cortex.

1. An 8 x 8-channel microelectrode array was used to map epicortical field potentials from a 4.375 x 4.375-mm2 area in the right parietotemporal neocortex of four rats. Potentials were evoked with bilaterally presented click stimuli and with electrical stimulation of the ventral and dorsal divisions of the medial geniculate body. 2. Epicortical responses to click stimuli replicated earlier findings. The responses consisted of a positive-negative biphasic waveform (P1a and N1) in the region of primary auditory cortex (area 41) and a positive monophasic waveform (P1b) in the region of secondary auditory cortex (area 36). Two potential patterns, one at the latency of the N1 and the other at the latency of the P1b, were used to represent activation of cells within areas 41 and 36. A linear combination of these patterns was sufficient to explain from 90 to 94% of the variance of the evoked potential complex at all latencies. 3. In the same animals, epicortical responses to electrical stimulation of the ventral and dorsal divisions of the medial geniculate body were also localized to areas 41 and 36, respectively. A linear combination of potential patterns from these separate stimulation conditions was sufficient to explain from 80 to 93% of the variance of the original click-evoked potential complex at all latencies. 4. These data provide functional evidence for anatomically defined topographical thalamocortical projections to primary and secondary auditory cortex. They suggest that short-latency cortical evoked potentials (10-60 ms poststimulus) are dominated by parallel thalamocortical activation of areas 41 and 36.

No abstract