STIMULUS-DEPENDENT MODULATION OF SPIKE BURST LENGTH IN CAT STRIATE CORTICAL-CELLS

Burst activity, defined by groups of two or more spikes with intervals of less than or equal to 8 ms, was analyzed in responses to drifting sinewave gratings elicited from striate cortical neurons in anesthetiz ed cats. Bursting varied broadly across a population of 507 simple and complex cells. Half of this population had greater than or equal to 4 2% of their spikes contained in bursts. The fraction of spikes in burs ts did not vary as a function of average firing rate and was stationar y over time. Peaks in the interspike interval histograms were found at both 3-5 ms and 10-30 ms. In many cells the locations of these peaks were independent of firing rate, indicating a quantized control of fir ing behavior at two different time scales. The activity at the shorter time scale most likely results from intrinsic properties of the cell membrane, and that at the longer scale from recurrent network excitati on. Burst frequency (bursts per s) and burst length (spikes per burst) both depended on firing rate. Burst frequency was essentially linear with firing rate, whereas burst length was a nonlinear function of fir ing rate and was also governed by stimulus orientation. At a given fir ing rate, burst length was greater for optimal orientations than for n onoptimal orientations. No organized orientation dependence was seen i n bursts from lateral geniculate nucleus cells. Activation of cortical contrast gain control at low response amplitudes resulted in no burst length modulation, but burst shortening at optimal orientations was f ound in responses characterized by supersaturation. At a given firing rate, cortical burst length was shortened by microinjection of gamma-a minobutyric acid (GABA), and bursts became longer in the presence of N -methyl-bicuculline, a GABA(A) receptor blocker. These results are con sistent with a model in which responses are reduced at nonoptimal orie ntations, at least in part, by burst shortening that is mediated by GA BA. A similar mechanism contributes to response supersaturation at hig h contrasts via recruitment of inhibitory responses that are tuned to adjacent orientations. Burst length modulation can serve as a form of coding by supporting dynamic, stimulus-dependent reorganization of the effectiveness of individual network connections.