In the vestibular nuclei, acute
hypotension induces excitation of electrical activity and expression of
c-Fos protein and phosphorylated
extracellular signal-regulated kinase (pERK). Expression of
c-Fos protein and pERK is mediated by the excitatory
neurotransmitter,
glutamate. We investigated the signaling pathway of
glutamate and its receptors in the vestibular nuclei following acute
hypotension in conscious rats.
Glutamate release and the expression of
c-Fos protein in the medial vestibular nuclei (MVN) were measured by microdialysis and immunohistochemical analysis, respectively. We compared the responses of rats with unilateral labyrinthectomy to unaltered controls. Acute
hypotension was induced by infusing
sodium nitroprusside (SNP) into the femoral vein. In the control group,
glutamate release and the expression of
c-Fos protein increased in the bilateral MVN following acute
hypotension. In the unilateral labyrinthectomy group,
glutamate release and the expression of
c-Fos protein increased in the MVN contralateral to the lesion, but did not change in the ipsilateral MVN following acute
hypotension. Microinjection of
NMDA or
AMPA into the lateral ventricle increased the expression of
c-Fos protein in the bilateral MVN of conscious intact labyrinthine rats. However, after intracerebroventricular microinjection of
MK-801 or
CNQX little
c-Fos protein was expressed in the bilateral MVN of these rats following acute
hypotension. These results suggest that in response to acute
hypotension, excitatory afferent signals from the peripheral vestibular receptors release
glutamate into postsynaptic neurons in the vestibular nuclei. These excitatory signals are transmitted through the
NMDA receptors and
AMPA receptors of
glutamate in the vestibular system.