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 preload the tissue. Results demonstrate that the 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.