GABA affects the release of gastrin and somatostatin from rat antral mucosa

Abstract

γ-Aminobutyric acid (GABA) is regarded as the major inhibitory neurotransmitter in the central nervous system of vertebrates^1–3. GABA exerts its inhibitory actions by interacting with specific receptors on pre- and postsynaptic membranes^4–6 and has been shown to inhibit somatostatin release from hypothalamic neurones in vitro⁷. Concepts of innervation of the gastrointestinal tract⁸ have been expanded by recent studies which suggest that GABAergic neurones are not confined solely to the central nervous system but may also exist in the vertebrate peripheral autonomic nervous system⁹. Jessen and coworkers^9,10 have demonstrated the presence, synthesis and uptake of GABA by the myenteric plexus of the guinea pig taenia coli, and have documented the presence of glutamic acid decarboxylase(GAD) in isolated myenteric plexus. This enzyme is responsible for the conversion of glutamic acid to GABA in GABAergic neurones. The possibility that GABA may have a role in neurotransmission or neuromodulation in the enteric nervous system of the vertebrate gut has been suggested by several investigators^11–13. Furthermore, GABA receptors have been demonstrated on elements of the enteric nervous system^14,15. The effects of GABA on gastrointestinal endocrine cell function have not been examined. We report here the effects of GABA on gastrin and somatostatin release from isolated rat antral mucosa in short-term in vitro incubations.