Adenosine operating in the nucleus of the solitary tract (NTS) may inhibit or facilitate neurotransmitter release from nerve terminals and directly inhibit or facilitate central neurons via A 1 and A 2a pre‐ and postsynaptic receptors, respectively. However, adenosine A 2a receptors, may also activate GABA‐ergic neurons/terminals which in turn inhibit glutamatergic transmission in the NTS network. Our previous studies showed that adenosine operating via both A 1 (inhibitor) and A 2a (activator) receptors powerfully inhibits the cardiopulmonary chemoreflex ( CCR) at the level of the caudal NTS. A 1 receptors most likely inhibit glutamate release in the CCR network, whereas A 2a receptors facilitate NTS GABA‐ergic mechanisms which in turn inhibit CCR glutamatergic transmission. Therefore, we hypothesized that A 2a receptors are located on NTS GABA‐ergic neurons/terminals whereas A 1 receptors may be located on NTS glutamatergic neurons/terminals. We investigated this hypothesis using double immunofluorescent staining for A 2a or A 1 adenosine receptors and GABA synthesizing enzyme, GAD67, in 30 μm thick, floating, medullary rat sections. We found that A 2a adenosine receptors are localized within the GABA‐ergic cells in the caudal NTS, whereas A 1 adenosine receptors are absent from these neurons. Instead, A 1 receptors were located on non‐ GABA‐ergic (likely glutamatergic) neurons/terminals in the caudal NTS. These data support our functional findings and the hypothesis that adenosine A 2a, but not A 1 receptors are located on GABA‐ergic neurons.