In vivo release by vagal stimulation of L-[3H] glutamic acid in the nucleus tractus solitarius preloaded with L-[3H] glutamine.

In anesthetized and paralyzed rats, using a push-pull perfusion technique, we examined the effect of bilateral vagal stimulation on the release of L-[3H] glutamic acid (L- [3H] Glu) from the nucleus tractus solitarius (NTS), after preloading the tissue either with L-[3H] Glu or L-[3H] glutamine (L- [3H] Gln). Vagal stimulation sufficient to produce a maximum fall of arterial pressure (AP) evoked release of L- [3H] Glu from the NTS when the tissue was preloaded with either 3H-Glu or 3H-Gln, and of D-[3H] aspartic acid (D-[3H] Asp) when this stable Glu analogue was used to preloaded with either 3H-Glu or 3H-Gln, and of D-[3H] precursor L-Gln is a good marker of the releasable pool of L-Glu in vivo and are consistent with the hypothesis that L-[3H] Glu is a neurotransmitter in the NTS, mediating the vasodepressor response from cardiopulmonary mechanoreceptors.