1. We sought first to determine whether neurones in caudomedial aspects of commissural nucleus tractus solitarii (NTS) received input from cardiopulmonary C fibre endings supplied by the pulmonary versus systemic circulation. We then examined the role of N-methyl-Daspartate (NMDA) and non-NMDA receptors in transmitting cardiopulmonary C fibre input to such NTS neurones. 2. Extracellular NTS unit activity, phrenic nerve activity and arterial blood pressure were recorded in urethane-anaesthetized rats. Unit responses to right atrial and left ventricular phenylbiguanide injections were compared in rats with arterial baroreceptors, carotid chemoreceptors and subdiaphragmatic vagal inputs eliminated. Right atrial phenylbiguanide injections produced greater peak responses (27 + 11 impulses s-) than did left ventricular injections (11 + 3 impulses s-') (n = 9).3. The non-NMDA receptor agonist quisqualic acid (QUIS) and NMDA were ionophoresed onto NTS neurones that were synaptically activated by right atrial phenylbiguanide injection.Responses were compared before and during ionophoresis of the non-NMDA receptor antagonist 2,3-dihydroxy-6-nitro-7-sulphamoylbenzo(f)quinoxaline (NBQX), the NMDA receptor antagonist DL-2-amino-5-phosphovaleric acid (AP5), or the broad spectrum antagonist kynurenic acid (KYN). 4. NBQX, which blocked QUIS-but spared NMDA-evoked responses, significantly attenuated synaptic activation by 65 % (n = 9). AP5, which blocked NMDA-but spared QUIS-evoked responses, did not significantly diminish synaptic activation (11 %; n = 7). KYN, which blocked QUIS-and NMDA-evoked responses, decreased synaptic activation by 70 % (n = 9). 5. The results suggest that input from cardiopulmonary C fibre endings, primarily supplied by the pulmonary circulation, is transmitted to this commissural NTS region largely via non-NMDA receptors.

1. We examined the effects of cigarette smoke, inhaled alone and during mild pulmonary venous congestion, on the activity of fifty-three neurones in the nucleus tractus solitarii (NTS) that were excited by input from pulmonary rapidly adapting receptors (RAR). Ten neurones excited by slowly adapting stretch receptors (SAR) were also studied. 2. Extracellular recordings of RAR-activated neurones were recorded in a-chloralose anaesthetized rabbits. Smoke from low-and high-nicotine cigarettes was delivered through a ventilator. Mild pulmonary venous congestion was produced by inflating a balloon in the left atrium. 3. Inhalation of three breaths of smoke from low-nicotine cigarettes increased the activity of fifty-one out of fifty-three RAR-activated neurones from 5.9 + 1 0 to 14'4 + 2-1 spikes breath' (P < 005).4. The responses of fifteen neurones were compared with smoke inhaled alone or during mild pulmonary venous congestion. Smoke alone increased unit activity from 6'8 + 2-3 to 12-6 + 3-7 spikes breath-' (P< 0 05). Small increases in left atrial pressure (2-0 + 0'5 mmHg) had no effect on baseline unit activity (7X6 + 2X11 vs. 7'7 + 2-3 spikes breath-'; P> 0 05), but enhanced the responses to smoke, increasing the activity from 7'6 + 2'1 to 17-1 + 4'8 spikes breath-' (P< 0 05). The response was greater than to smoke alone (P < 0 05).5. Of ten SAR-activated neurones, seven failed to respond to inhaled cigarette smoke, two were excited and one was inhibited. Pulmonary venous congestion had no effect on the unit activity before and after smoke (n = 4 neurones). 6. We conclude that smoke-evoked excitation of RAR lower-order neurones is augmented by pulmonary venous congestion.