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.
D000344:Afferent Pathways / Q000502:physiology; D000818:Animals; D001345:Autoradiography; D004558:Electric Stimulation; D005971:Glutamates / Q000378:metabolism*; D018698:Glutamic Acid; D005973:Glutamine / Q000378:metabolism*; D008526:Medulla Oblongata / Q000502:physiology*; D010477:Perfusion; D051381:Rats; D011919:Rats, Inbred Strains; D014316:Tritium; D014630:Vagus Nerve / Q000502:physiology*
D005971:Glutamates; D005973:Glutamine; D014316:Tritium; D018698:Glutamic Acid