Abstract

Several available reports demonstrate the presence of infraslow activity (< 0.5 Hz) in structures of the auditory system of the brain. It was reported earlier that specific alterations of this activity in the domain of seconds (0.1–0.5 Hz) occurred in the medial geniculate nucleus (MGN) and primary auditory cortex (A1) in response to acoustic stimuli. The present study was performed to test two hypotheses: (1) that potentials in the domain of seconds (0.1–0.5 Hz) reflect specific and direct interactions of the MGN and A1 during neural processing of sensory information, and (2) that low-frequency infraslow potentials in the A1 (< 0.1 Hz) are related to brainstem influences originating from the locus coeruleus (LC) and dorsal raphe nucleus (DRN). The experimental subjects were 25 adult rats with chronic stereotaxic electrodes implanted in the MGN, A1, LC, and DRN. The animals were anesthetized and infraslow activity was once recorded under several experimental conditions: (1) in the A1 before and after electrical stimulation of MGN, (2) in the A1 before and after electrical stimulation of LC, and (3) in the A1 before and after electrical stimulation of DRN. The effects of MGN stimulation were limited to overall increases in spectral power in the frequency domain of 0.1–0.5 Hz. Specifically, power increased in the frequencies of 0.1–0.25, 0.35–0.4, and 0.45–0.5 Hz in the A1 after MGN stimulation. The electrical stimulation of either the LC or DRN affected only multisecond activity (0.0167–0.04 Hz) in the A1 in the similar way (increase of powers of multisecond potentials), but it does not induced any changes in the activity with the frequencies of 0.1–0.5 Hz in this structure. These results support tentative conclusions that infraslow activity in the range of 0.1–0.5 Hz is implicated in specific mechanisms of interactions within the MGN-A1 thalamic–cortical system, whereas multisecond potentials (0.0167–0.04 Hz) in A1 are mainly attributed to the influences of brainstem nuclei (like LC and DRN) on general neuronal excitability of this auditory cortical area.

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