Abstract
Many cases of hearing loss have been reported in victims of Minamata disease, caused by methylmercury poisoning. Thiophene, like methylmercury, induces cerebellar granule cell degeneration in rats. To investigate the pathophysiology of the central auditory system in thiophene-poisoned rats, spontaneously hypertensive rats stroke resistance (SHR·SR) were given 0.15ml of thiophene daily for 5 or 6 days. After the rats had undergone brainstem recording and analysis of the auditory brainstem response (ABR), they were necropsied for histopathological examination. In the thiophene-poisoned animals, an abnormal ABR pattern like that in methylmercury poisoning appeared. In the acute stage, by 5 days after administration (DAA), the IV wave amplitude was reduced and the interpeak latency (IPL) was prolonged to various degrees. At 5 DAA, the IPL returned to the pretreatment level, earlier than the amplitude. In rats with severe cerebellar injury, a PAS-positive substance was localized in the inferior colliculus, comprising the central nucleus, and especially its ventrolateral portion. The lesions included neuronal necrosis, edema of the neuropil, and axonal degeneration. Proliferated GFAP-positive cells were located close to areas of neuronal loss. Our results suggest that demonstration of ABR is useful for evaluating disturbance of the central auditory system induced by chemicals.
