As previously demonstrated, spontaneously firing bulbar inspiratory neurones are periodically inhibited either at the beginning of, or throughout expiration, while bulbar expiratory neurones are inhibited during inspiration. The aim of the present study was to test the hypothesis that amino acids act as transmitters of these periodic inhibitions. The study was performed using iontophoretic applications of drugs on bulbar respiratory neurones. On these neurones GABA and glycine-sensitive sites were identified and differentiated on the basis of the actions of agonist (muscimol) or antagonists (bicuculline, picrotoxin and strychnine). Using competitive antagonists (nipecotic acid, beta-alanine) mechanisms responsible for GABA uptake were found in the close vicinity of respiratory-related neurones. Some but not all types of periodic inhibition were found to be reduced following application of GABA or glycine antagonists. Strychnine was found to reduce periodic inhibitions occurring at the beginning of expiration in inspiratory neurones. GABA antagonists had an effect on those periodic depressions which were prolonged throughout expiration. A different and complementary role of glycine-like and GABA-like systems in central respiratory mechanisms is proposed.