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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.

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The purpose of this study was to use depth electrical stimulation and retrograde horseradish peroxidase (HRP) labeling to determine what role certain subcortical nuclei play in the neurogenesis of high-frequency gamma (approximately 40 Hz) oscillations in rat auditory cortex. Evoked and spontaneous electrocortical oscillations were recorded with the use of a high-spatial-resolution multichannel epipial electrode array while electrical stimulation was delivered to the posterior intralaminar (PIL) region of the ventral acoustic thalamus and to the centrolateral nucleus (CL) and the nucleus basalis (NB), which have been previously implicated in the production of cortical gamma oscillations. PIL stimulation consistently evoked gamma oscillations confined to a location between primary and secondary auditory cortex, corresponding to the region where spontaneous gamma oscillations were also recorded. Stimulation of the CL and NB did not evoke gamma oscillations in auditory cortex. HRP placed in the cortical focus of evoked gamma oscillations labeled cell bodies in the PIL, and in more lateral regions of the ventral acoustic thalamus, which on subsequent stimulation also evoked gamma oscillations in auditory cortex. No cells were labeled in either the CL or NB. These results indicate that the PIL and the lateral regions of ventral acoustic thalamus provide anatomically distinct input to auditory cortex and may play an exclusive and modality-specific role in modulating gamma oscillations in the auditory system.