Abstract
The purpose of current study was to elucidate whether vestibulocerebellar N-methyl- d-aspartate (NMDA) receptors are implicated in MK801 induced vestibular decompensation. Sprague–Dawley rats were unilaterally labyrinthectomized (ULX) and some of them were uvulonodullectomized before ULX (UNL+ULX). Number of spontaneous nystagmus (SN) and degree of head deviation (HD) were used as a parameter of behavioral recovery. MK801 treatment 6 h after ULX produced significant increases in SN and decreased HD in ULX rats, indicating decompensation. In marked contrast, however, MK801 treatment resulted in a great reduction of SN and HD in UNL+ULX rats, suggesting involvement of vestibulocerebellar NMDA receptors in MK801 induced decompensation during early stage of vestibular compensation.
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