Figure 1.

Summary schematic diagram illustrating the prominent role of brainstem GABAergic transmission in regulating vago-vagal reflex control of the stomach. Vagal afferent (sensory; blue) fibers innervating the GI tract transduce and relay signals centrally; the cell bodies of these sensory neurons lie within the paired nodose ganglia and their central terminals enter the brainstem via the tractus solitarius and terminate within the nucleus tractus solitarius (NTS) using predominately glutamate (Glu; green) as their neurotransmitter. NTS neurons integrate these visceral sensory signals with those from other brainstem and higher CNS nuclei involved in autonomic homeostatic control and relay the integrated signal to the adjacent dorsal motor nucleus of the vagus (DMV) using Glu and GABA (red) as neurotransmitters. The critical role of GABAergic signaling to regulate DMV neuronal activity is illustrated by the accompanying gastric motility traces, recorded using miniaturized strain gauges affixed to the ventral surface of the gastric corpus. Note that following microinjection of the non-selective ionotropic glutamate antagonist, kynurenic acid, there was very little change in gastric motility or tone. In contrast, following microinjection of the GABA_A receptor antagonist, bicuculline, gastric motility and tone increased dramatically, demonstrating that DMV neurons are under a tonic inhibitory, GABAergic drive.²⁷ (A color version of this figure is available in the online journal.)