Excitatory pathways from the vestibular nuclei to the NTS and the PBN and indirect vestibulo-cardiovascular pathway from the vestibular nuclei to the RVLM relayed by the NTS.

Previous studies have confirmed the existence of vestibulo-sympathetic pathways in the central nervous system. However, the exact pathways and neurotransmitters underlying this reflex are unclear. The present study was undertaken to investigate whether the vestibulo-cardiovascular responses are a result of activated glutamate receptors in the caudal vestibular nucleus. We also attempt to verify the indirect excitatory pathways from the vestibular nucleus (VN) to the rostral ventrolateral medulla (RVLM) using a tracing method combined with a vesicular glutamate transporter (VGluTs) immunofluorescence. In anesthetized rats, unilateral injection of l-glutamate (5 nmol) into the medial vestibular nucleus (MVe) and spinal vestibular nucleus (SpVe) slightly increased the mean arterial pressure (MVe: 93.29+/-11.58 to 96.30+/-11.66, SpVe: 91.72+/-15.20 to 95.48+/-17.16). Local pretreatment with the N-methyl-D-aspartate (NMDA)-receptor antagonist MK-801 (2 nmol) significantly attenuated the pressor effect of L-glutamate injected into the MVe compared to the contralateral self-control. After injection of biotinylated dextran amine (BDA) into the MVe and SpVe, and fluorogold (FG) into the RVLM, some BDA-labeled fibres and terminals in the nucleus of solitary tract (NTS) and the parabrachial nucleus (PBN) were immunoreactive for VGluT1 and VGluT2. Several BDA-labeled fibres were closely apposed to FG-labeled neurons in the NTS. These results suggested that activation of caudal vestibular nucleus neurons could induce pressor response and NMDA receptors might contribute to this response in the MVe. The glutamatergic VN-NTS and VN-PBN pathways might exist, and the projections from the VN to the RVLM relayed by the NTS comprise an indirect vestibulo-cardiovascular pathway in the brain stem.