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We investigated the changes in glutamate release from the ipsi- and contra-lesional medial vestibular nucleus (MVN) following unilateral labyrinthectomy (UL) by in vivo microdialysis study. The concentration of glutamate in the ipsi-lesional MVN was decreased until 4 h. Twelve hours after UL, the concentration of glutamate was restored back to the basal level, after which the release did not show any change between 24 and 48 h post-UL. In contrast, the concentration of glutamate in the contra-lesional MVN, which increased immediately after UL, decreased gradually to the basal level until 3–4 h post-UL, followed by no further change. The difference in the glutamate concentration between ipsi- and contra-lesional MVN increased immediately after UL and gradually decreased accompanied by a reduction in the frequency of nystagmus, although spontaneous nystagmus had not disappeared by the time the imbalance of glutamate release diminished. These results suggest that the imbalance of glutamate release between bilateral nuclei induced the nystagmus, and the change in release is concerned with the rapid development of vestibular compensation. [Copyright &y& Elsevier]

The function of the 5-hydroxytryptamine (5-HT) system in the medial vestibular nucleus (MVN) was evaluated using KCl-evoked 5-HT release assessed by in vivo microdialysis. The release of 5-HT in the MVN was increased by the local application of KCl (100 mM) in a calcium-dependent manner. Likewise, perfusion of a 5-HT reuptake blocking agent, clomipramine (1 μM), increased extracellular levels of 5-HT in the MVN. Finally, pretreatment with the selective 5-HT1A agonist, 8-hydroxy-2-(di-N-propylamino) tetralin (1 mg/kg, intraperitoneally), attenuated the KCl-evoked 5-HT release. These findings suggest that 5-HT stored in vesicles is released from nerve terminals in the MVN. In addition, its regulation may be mediated by control of somatodendritic 5-HT1A receptor activation. [Copyright &y& Elsevier]