Inter- and intra-hemispheric spatiotemporal organization of spontaneous electrocortical oscillations.

1. Two 64-channel epipial electrode arrays were positioned on homologous locations of the right and left hemisphere, covering most of primary and secondary auditory and somatosensory cortex in eight lightly anesthetized rats. Array placement was verified with the use of cytochrome oxidase histochemistry. 2. Middle-latency auditory and somatosensory evoked potentials (MAEPs and MSEPs, respectively) and spontaneous oscillations in the frequency range of 20-40 Hz (gamma oscillations) were recorded and found to be spatially constrained to regions of granular cortex, suggesting that both phenomena are closely associated with sensory information processing. 3. The MAEP and MSEP consisted of an initial biphasic sharp wave in primary auditory and somatosensory cortex, respectively, and a similar biphasic sharp wave occurred approximately 4-8 ms later in secondary sensory cortex of the given modality. Averaged gamma oscillations also revealed asynchronous activation of sensory cortex, but with a shorter 2-ms delay between oscillations in primary and secondary regions. Although the long latency shift of the MAEP and MSEP may be due in part to asynchronous activation of parallel thalamocortical projections to primary and secondary sensory cortex, the much shorter shift of gamma oscillations in a given modality is consistent with intracortical coupling of these regions. 4. Gamma oscillations occurred independently in auditory and somatosensory cortex within a given hemisphere. Furthermore, time series averaging revealed that there was no phase-locking of oscillations between the sensory modalities. 5. Gamma oscillations were loosely coupled between hemispheres; oscillations occurring in auditory or somatosensory cortex of one hemisphere were often associated with lower-amplitude oscillations in homologous contralateral sensory cortex. Yet, the fact that time series averaging revealed no interhemispheric phase-locking suggests that the corpus callosum may not coordinate the bilateral gamma oscillations, and that a thalamic modulatory influence may be involved.