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.