We investigated whether stimulation of the pyramidal tract (PT) could reset the phase of 15‐30 Hz beta oscillations observed in the macaque motor cortex. We recorded local field potentials (LFPs) and multiple single‐unit activity from two conscious macaque monkeys performing a precision grip task. EMG activity was also recorded from the second animal. Single PT stimuli were delivered during the hold period of the task, when oscillations in the LFP were most prominent. Stimulus‐triggered averaging of the LFP showed a phase‐locked oscillatory response to PT stimulation. Frequency domain analysis revealed two components within the response: a 15‐30 Hz component, which represented resetting of on‐going beta rhythms, and a lower frequency 10 Hz response. Only the higher frequency could be observed in the EMG activity, at stronger stimulus intensities than were required for resetting the cortical rhythm. Stimulation of the PT during movement elicited a greatly reduced oscillatory response. Analysis of single‐unit discharge confirmed that PT stimulation was capable of resetting periodic activity in motor cortex. The firing patterns of pyramidal tract neurones (PTNs) and unidentified neurones exhibited successive cycles of suppression and facilitation, time locked to the stimulus. We conclude that PTN activity directly influences the generation of the 15‐30 Hz rhythm. These PTNs facilitate EMG activity in upper limb muscles, contributing to corticomuscular coherence at this same frequency. Since the earliest oscillatory effect observed following stimulation was a suppression of firing, we speculate that inhibitory feedback may be the key mechanism generating such oscillations in the motor cortex.

Recently, it has been proposed that all suppressive phenomena observed in the primary visual cortex (V1) are mediated by a single mechanism, involving inhibition by pools of neurons, which, between them, represent a wide range of stimulus specificities. The strength of such inhibition would depend on the stimulus that produces it (particularly its contrast) rather than on the firing rate of the inhibited cell. We tested this hypothesis by measuring contrast-response functions (CRFs) of neurons in cat V1 for stimulation of the classical receptive field of the dominant eye with an optimal grating alone, and in the presence of inhibition caused by (1) a superimposed orthogonal grating (cross-orientation inhibition); (2) a surrounding iso-oriented grating (surround inhibition); and (3) an orthogonal grating in the other eye (interocular suppression). We fitted hyperbolic ratio functions and found that the effect of cross-orientation inhibition was best described as a rightward shift of the CRF (‘contrast-gain control’), while surround inhibition and interocular suppression were primarily characterised as downward shifts of the CRF (‘response-gain control’). However, the latter also showed a component of contrast-gain control. The two modes of suppression were differently distributed between the layers of cortex. Response-gain control prevailed in layer 4, whereas cells in layers 2/3, 5 and 6 mainly showed contrast-gain control. As in human observers, surround gratings caused suppression when the central grating was of high contrast, but in over a third of the cells tested, enhanced responses for low-contrast central stimuli, hence actually decreasing threshold contrast.

FOR the majority of neurones in cat striate cortex, the response to an optimal stimulus presented to one eye is suppressed when a stimulus of substantially different orientation is presented to the other eye. In order to determine the true orientational tuning of the underlying inhibitory interactions in the absence of binocular facilitation for matched stimuli, we tested how the response of such cells to an optimal grating in one eye is affected by gratings in the other eye of spatial frequencies too high or low to elicit an excitatory response through either eye: the vast majority of cells displayed suppression that was essentially independent of orientation. Our results indicate that interocular inhibition derives from cells representing all orientations, but is swamped by interocular facilitation for stimuli matched in orientation and spatial frequency.