MICROINJECTION OF GLYCINE INTO THE NUCLEUS AMBIGUUS ELICITS TACHYCARDIA IN SPINAL RATS

In 30 male Wistar spinal (C1) rats, anaesthetized with urethane and artificially ventilated, experiments were done to study the effect on heart rate (HR) and arterial pressure (AP) of microinjection of the inhibitory amino acid glycine (Gly) into the nucleus ambiguus (NA). L-Glutamate (Glu; 1.5 nmol) was microinjected into the region of the right NA to search for sites from which decreases in AP and HR could be elicited. The decreases in HR were found to be 73.1 +/- 7.0 bpm (n = 30). No changes in AP were observed. Microinjection of Gly (1 M; 2-20 nmol in 2-20 nl; n = 12) elicited a dose dependent increase in HR with no changes in AP. Microinjection of Gly 1-2 min before microinjection of Glu in 7 sites reduced significantly (P < 0.05) the decrease in HR elicited by Glu from 87.0 +/- 27.3 bpm to 17.7 +/- 7.2 bpm. Increases in HR elicited by Gly in the right NA of another 12 rats were not affected significantly by prior microinjection of the Gly antagonist strychine hydrochloride (30-90 pmol in 10-30 nl in one group of animals, n = 6; and 2.5 nmol in 50 nl in another group, n = 6). In addition, to determine whether the effects of Gly were caused by actions on N-methyl-D-aspartate (NMDA) receptors, kynurenic acid (KYN; 4.5 nmol in 30 nl) was microinjected into the right NA of 6 rats prior to microinjection of Gly. KYN failed to block the response to Gly microinjection and instead potentiated the HR increase elicited by Gly. These results suggest that Gly acts as an inhibitory amino acid transmitter influencing vagal neurons in the right NA controlling HR and that the effects of Gly are mediated probably through strychnine-insensitive non-NMDA receptors.