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γ-Aminobutyric Acid (GABA) and its receptors, GABA A,B,C , are expressed in several locations along the gastrointestinal tract. Nevertheless, a role for GABA in enteric synaptic transmission remains elusive. In this study, we characterized the expression and function of GABA in the myenteric plexus of the mouse ileum. About 8% of all myenteric neurons were found to be GABA-immunoreactive (GABA+) including some Calretinin+ and some neuronal nitric oxide synthase (nNOS+) neurons. We used  Wnt1-Cre;R26R-GCaMP3  mice, which express a genetically encoded fluorescent calcium indicator in all enteric neurons and glia. Exogenous GABA increased the intracellular calcium concentration, [Ca 2+ ] i  of some myenteric neurons including many that did not express GABA or nNOS (the majority), some GABA+, Calretinin+ or Neurofilament-M (NFM)+ but rarely nNOS+ neurons. GABA+ terminals contacted a significantly larger proportion of the cell body surface area of Calretinin+ neurons than of nNOS+ neurons. Numbers of neurons with GABA-induced [Ca 2+ ] i  transients were reduced by GABA A,B,C  and nicotinic receptor blockade. Electrical stimulation of interganglionic fiber tracts was used to examine possible effects of endogenous GABA release. [Ca 2+ ] i  transients evoked by single pulses were unaffected by specific antagonists for each of the 3 GABA receptor subtypes. [Ca 2+ ] i  transients evoked by 20 pulse trains were significantly amplified by GABA C  receptor blockade. These data suggest that GABA A  and GABA B  receptors are not involved in synaptic transmission, but suggest a novel role for GABA C  receptors in modulating slow synaptic transmission, as indicated by changes in [Ca 2+ ] i  transients, within the ENS.

frontiers in physiology

Neurally Released GABA Acts via GABAC Receptors to Modulate Ca2+ Transients Evoked by Trains of Synaptic Inputs, but Not Responses Evoked by Single Stimuli, in Myenteric Neurons of Mouse Ileum