The purpose of our study was to determine whether taurine, like other naturally occurring central nervous system amino acid neurotransmitters (e.g., gamma-aminobutyric acid and glycine), act at the ventral surface of the medulla to influence cardiorespiratory activity. This was accomplished by monitoring cardiorespiratory activity. This was accomplished by monitoring cardiorespiratory activity in chloralose-anesthetized cats and then applying several doses of taurine locally to the ventral medullary surface chemosensitive areas. We found that 2 and 4 mumol of taurine applied to the intermediate area of the ventral surface produced cardiorespiratory depression, whereas taurine, in a similar dose range, produced only respiratory depression when applied to the rostral area. In contrast, taurine applied to the caudal area had no cardiorespiratory effects. Similar experiments with glycine revealed that this inhibitory amino acid elicited a similar pattern of cardiorespiratory depression as taurine. Furthermore, strychnine, an antagonist of glycine, counteracted the cardiorespiratory depressant effects of both taurine and glycine effectively. Pretreatment with strychnine prevented most of the cardiorespiratory depressant effects of taurine and glycine. 6-Aminomethyl-3-methyl-4H-1, 2,4-benzothiadiazine-1,1-dixoide, a putative antagonist of taurine, had antagonistic effects similar to those of strychnine in both treatment and pretreatment studies. 6-Aminomethyl-3-methyl-4H-1,2,4-benzothiadiazine-1,1-dioxide, per se, increased tidal volume when applied to the intermediate area; strychnine had no effect. These results indicate that taurine acts at the chemosensitive areas on the ventral surface of the medulla to produce cardiorespiratory depression, and these effects are due to an interaction of taurine with receptors similar to, but probably not identical with, glycine receptors.