1 The respiratory response to microinjection of capsaicin into the commissural nucleus of the solitary tract (cNTS) of urethane-anaesthetized rats was investigated in the absence and presence of the competitive vanilloid (capsaicin) antagonist, capsazepine, and selective tachykinin NK 1 , NK 2 and NK 3 antagonists (RP 67580, SR 48968 and SR 142801, respectively). 2 Microinjection of capsaicin reduced respiratory frequency but not tidal volume (VT), leading to an overall reduction in minute ventilation (V . E). The eect was dose-dependent between 0.5 and 2 nmol capsaicin. Doses greater than 2 nmol produced apnoea. Tachyphylaxis was observed following repeated injection of capsaicin (1 nmol, 30 min apart). 3 Capsazepine (1 nmol) had no eect on frequency or VT when injected alone but completely blocked the respiratory response to capsaicin (1 nmol). 4 RP 67580 (1 but not 5 nmol) alone depressed frequency and VT slightly. Moreover, RP 67580 appeared to potentiate the bradypnoeic eect of capsaicin. In contrast, SR 48968 and SR 142801 (1 and 5 nmol) alone had no signi®cant eect on respiration. However, both agents signi®cantly attenuated the reduction in frequency produced by capsaicin. 5 In conclusion, microinjection of capsaicin into the cNTS decreases overall ventilation, primarily by reducing frequency. The action of capsaicin appears from the data to be mediated by vanilloid receptors since it is blocked by the competitive vanilloid antagonist capsazepine and is subject to tachyphylaxis. However, since NK 2 (SR 48968) and NK 3 (SR 142801) receptor antagonists block the actions of capsaicin, we propose that capsaicin acts also by releasing tachykinins from central aerent terminals in the cNTS.