NMDA RECEPTOR SUBUNIT NR1-IMMUNOREACTIVITY IN THE RAT PONS AND BRAIN-STEM AND COLOCALIZATION WITH FOS INDUCED BY NASAL STIMULATION

In the present study, we examined the distribution of neurons in the p arabrachial nucleus (PB), the Kolliker-Fuse nucleus (KF), the spinal t rigeminal nucleus caudalis (Sp5C), the nucleus of the solitary tract ( NTS) and the ventrolateral medulla (VLM), which are activated by evoki ng the nasotrigeminal reflex and which exhibit immunoreactivity for th e N-methyl-D-aspartate (NMDA) receptor subunit NR1. By stimulating the nasal mucosa with saline, we induced the expression of the immediate early gene c-fos and combined the immunocytochemical detection of the Fos protein with the detection of the NR1 subunit. Cell counts reveale d that nasal stimulation, compared to anesthesia controls, resulted in highly significant increases (p less than or equal to 0.001) of Fos-i mmunoreactive (-ir) neurons in the midlevel KF, the external lateral P B, and the Sp5C. In the central lateral PB, the rostral ventrolateral medulla including the Botzinger/pre-Botzinger complex, and in the vent rolateral and commissural NTS the increases were only moderately signi ficant(p less than or equal to 0.05). With respect to the numbers of N R1-/Fos-ir double-labeled neurons, significant increases were only obs erved in a subset of these pontomedullary nuclei. Increases were highl y significant in the Sp5C (p less than or equal to 0.001) and the midl evel KF(p less than or equal to 0.01) and moderately significant (p le ss than or equal to 0.05) in the external lateral PB, Botzinger/pre-Bo tzinger complex, and ventrolateral NTS. The present study revealed tha t nasotrigeminally activated neurons in mandatory and potential relay sites of the nasotrigeminal reflex circuit express the NR1 subunit. Th is finding strongly suggests that NMDA-type glutamate receptors are in volved in the mediation of the nasotrigeminally evoked cardiovascular and respiratory responses. (C) 1998 Elsevier Science B.V. All rights r eserved.