Prevention of vestibular deafferentation-induced spontaneous nystagmus with pretreatment of Ca2+ channel/N-methyl-D-aspartic acid receptor antagonists in guinea pigs.

Involvement of Ca2+ channel and N-methyl-D-aspartic acid (NMDA) receptors with induction of the spontaneous nystagmus (SN) after unilateral labyrinthectomy (UL) was evaluated by examining the effect of verapamil and MK-801 in guinea pigs. An injection of verapamil or MK-801 before the intratympanic application of arsanilate significantly (p < 0.05) suppressed the frequency of the SN towards the arsanilate-applied side. The frequency of the SN towards the intact side in these drug-treated animals was much lower than in the control animals until 36 h after the application of arsanilate. In addition, 60 days subsequent to induction of the UL, application of the drug before we injected the arsanilate into the opposite middle ear suppressed the SN towards the second arsanilate-injected side, but not towards the first injection side. We suggest that Ca2+ channel and NMDA receptor may be involved in the induction of the SN, and that the pretreatment of their antagonists could be applied in preventing the vestibular deafferentation-induced SN.