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hamsters, rats and chinchillas. This hyperactivity has been demonstrated to be correlated with the be- havioral evidence for tinnitus. It is conceivable that suppression of hyperactivity in the DCN would sup- press tinnitus. Somatosensory electrical stimulation (SES) has been used clinically to suppress tinnitus. However, due to a lack of understanding of the mechanisms of tinnitus suppression through SES, this approach has not been developed as an effective and reliable means for treating tinnitus. The current study was to test the effects of SES by delivering electrical current to the basal part of the pinna on DCN activity of both control and tone-exposed animals. Experiments were carried out in 26 adult hamsters, among which 13 were exposed to an intense tone under anesthesia (10 kHz tone, 125-130 dB SPL, 4 hrs) and another 13 age-matched control animals were similarly anesthetized but not exposed to a sound. One to three weeks after sound exposure and control treatment, multiunit activity was recorded at the surface of the left DCN before, during and after electrical stimulation of the left pinna. Electrical stimuli were single biphasic pulses of 200 us duration, delivered at 100-900 uA and 100 pps. The results from both control and exposed groups revealed four response types: S-S, referring to suppression during and after stimulation; E-S, manifesting excitation during stimulation but suppression after stimulation; S-E, showing suppression during stimulation but excitation after stimulation; E-E, representing excitation during and after stimulation. We found that there were more incidences of suppression than excitation during and after stimulation in both control and exposed groups. At higher levels of current, there was a significantly higher degree of suppression after stimulation than during stimulation for both groups, and there was also higher degree of suppression during and after stimulation in exposed animals than in controls. Our results are in line with previous clinical findings and support the view that DCN hyperactivity may be the direct neural cor- relate of tinnitus and suppression of DCN hyperactivity through SES may be one important approach in tinnitus suppression. (Supported by ATA).

GABAA Receptor Subunit Changes in a Noise-Exposure Model of Tinnitus: Rat Medial Geniculate Body. (Abstract of ARO Meeting Denver, Colorado) Donald Caspary1,2, Danyelle Martin3, Lynne Ling1, Hongning Wang1, Pete Hutson4, Jeremy Tur- ner2,5, Emma Reuschel6, Larry Hughes2 1Department of Pharmacology, Southern Illinois University School of Medicine, 2Department of Surgery/ Otolaryngology, Southern Illinois University School of Medicine, 3Department of Microbiology, University of Illinois at Chicago, 4Department of Sleep and Schizophrenia Research, Merck Inc., 5Department of Psychology, Illinois College, 6Department of Chemistry and Biology, Illinois College

The medial geniculate body (MGB) is the major auditory thalamic nucleus. MGB receives segregated as- cending inputs from the inferior colliculus and descending cortical inputs from auditory cortex and nonau- ditory cortices. Previous studies have reported noise-induced evidence of tinnitus in the central auditory system. The present study examined selective GABAA receptor subunit changes three months following a 16kHz octave-band, 115dB noise-exposure, thought to induce tinnitus in rats. Two non “wild-type” GABAA receptor subunits, the α4 and δ subunits appear to be concentrated in synaptic and extra-syn- aptic constructs in MGB. Subunit message levels were quantified using in situ hybridization and subunit proteins were visualized using fluorescent immunocytochemistry in young and aged noise-exposed rats compared to young and aged unexposed controls. Young noise-exposed rats showed significant upre- gulation of the α4 subunit in both ipsi- and contralateral MGB (>50% increase), while aged rats showed α4 subunit upregulation in the contralateral MGB (>100%increase). Young and aged noise-exposed rats showed significant δ subunit upregulation in the MGB (dorsal, young>48%; aged>103%; ventral, young>84%; aged>170%) contralateral to the noise exposure. It has been proposed (Sur et al., 1999) that upregulation of a α4βδ GABAA receptor construct may be a compensatory plastic change to offset hyperactive neuronal networks. The present GABAA receptor subunit changes suggest that noise exposure related changes in MGB may, in part, subserve the per

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