Release of [3H]L-glutamine acid (L-Glu) and [3H]D-aspartic acid (D-Asp) in the area of nucleus tractus solitarius in vivo produced by stimulation of the vagus nerve

We have investigated the effects of bilateral electrical stimulation of the vagus nerves in anesthetized, paralyzed rats on the release of exogenously administered [3H]L-glutamic acid ([3H]L-Glu) or [3H]D-aspartic acid ([3H]D-Asp) from the intermediate portion of the nucleus tractus solitarius (NTS). Electrical stimulation of afferent fibers with the frequency, pulse, duration, and intensity required to activate C-fibers, elicited hypotension and bradycardia. Such stimuli induced the release of [3H]L-Glu, or its stable analogue [3H]D-Asp, from the NTS into perfusate collected through push-pull cannulae. The release of radioactive materials, calculated as a percent of increase in radioactivity above the prestimulation level, was for [3H]L-Glu 114.4 +/- 25.1% (n = 20) during bilateral vagal stimulation, and 45.6 +/- 11.3% (n = 9) (P less than 0.001) during unilateral stimulation. The release of [3H]D-Asp induced by bilateral vagal stimulation was 100.4 +/- 31.9%. The release, which was anatomically specific and restricted to the NTS, was directly related to stimulus (and hence reflex) intensity. Overflow of the inert substances [14C]urea OR [14C]sucrose, co-administered with the [3H] amino acids, did not increase at the same time. Local depolarization of the cells in the NTS by K+ (53mM) increased the overflow of [3H]L-Glu, as well as [14C]urea, and was able to induce the release of [3H]L-Glu when electrical stimulation failed to have an effect. The results are consistent with the hypothesis that L-Glu is a neurotransmitter of neurons in the NTS mediating vasodepressor response from vagal afferents, including those from systemic baroreceptors.