Hypoxia induces c-Fos protein expression in NMDA but not AMPA glutamate receptor labeled neurons within the nucleus tractus solitarii of the conscious rat.

摘要

Glutamatergic transmission within the nucleus tractus solitarii (nTS) is critical to full expression of hypoxia-induced cardiorespiratory responses in the rat. To further examine the role of N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) glutamate receptors in these responses, double-labeling studies of immunoreactivity for c-Fos protein and either NMDA (NR1) or AMPA (mGluR2/3) receptor expression were conducted in normoxic rats and in hypoxic rats receiving vehicle, MK801, or NBQX. Hypoxia markedly increased c-Fos immunoreactivity within nTS neurons which in the vast majority co-labeled for NMDA. Furthermore, MK801 markedly attenuated such responses. In contrast, co-localization of AMPA and c-Fos occurred in only a small proportion of neurons, and NBQX failed to modify hypoxia-induced c-Fos enhancements. These data suggest a predominant role for NMDA but not for AMPA glutamate receptors in nTS mediated components of the hypoxic response.