The Bötzinger complex (BötC) is an important component of the respiratory network and one of the main source of inhibition for inspiratory activity. The specific role of inhibitory mechanisms within the BötC was investigated in a-chloralose-urethane anesthetized, vagotomized, paralysed and artificially ventilated rabbits by using bilateral microinjections (30-50 nl) of GABA and glycine receptor agonists and antagonists. GABA_A receptor blockade by bicuculline (5 mM) or gabazine (2 mM) induced strong depression of respiratory activity up to apnea. Glycine receptor blockade by strychnine (5 mM) induced mild decreases in both respiratory frequency and peak phrenic amplitude. GABA_B receptor blockade by CGP-35348 (50 mM) did not affect respiratory activity. Microinjections of the GABA_B receptor agonist baclofen (1 mM) increased respiratory frequency, without appreciable changes in peak phrenic amplitude. The results demonstrate that GABA and glycine receptors are expressed within the BötC of the rabbit. The effects induced by bicuculline and strychnine appear to be related to disinhibition of BötC inhibitory neurons. Thus, GABA_A and glycine receptors may have an intense modulatory role on inspiratory activity depending upon the inhibitory input they receive, with a major role played by GABA_A receptors. The source of inhibitory inputs to the BötC neurons remains to be investigated.