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Systemically Antagonizing L-Type Calcium Channels Modifies Intensity and Pattern of Fos Expression Evoked by Electrical Intracochlear Stimulation in the Adult Rat Auditory Brainstem

Peter Bischoff,Nicole Rosskothen-Kuhl*,Robert-Benjamin Illing*

Specific sensory activity such as sustained acoustical or Electrical Intracochlear Stimulation (EIS) elicits electrical responses and molecular changes in neuronal subpopulations of the auditory brainstem. One of the first molecular changes observed is the expression of the immediate early gene Fos. Its protein functions as a monomer of the transcription factor Activator Protein-1 (AP-1) which triggers cascades of protein synthesis that play a crucial role in neuroplastic remodeling. We investigated the pattern of Fos expression in Anteroventral (AVCN) and Dorsal Cochlear Nucleus (DCN) and Central Inferior Colliculus (CIC) following 2 h of unilateral EIS at 1.6, 50, and 400 Hz in anesthetized untreated and nimodipine-treated rats. Our data indicate that with increasing stimulation frequency the population of cells expressing Fos changed in composition and size in AVCN, DCN, and CIC. In all investigated auditory regions, systemic nimodipine treatment, an antagonist of L-type calcium channels, resulted in a significant increase in the number of neurons expressing Fos upon EIS compared to non-treated rats at the same stimulation parameters. Apparently, antagonizing L-type calcium channels enhances the responsiveness of neurons, and thus their readiness to respond with functional changes to sensory activity, in the auditory brainstem with little influence on the tonotopic precision of the response.