Electrophysiological effects of GABA on cat pancreatic neurons

In mammalian peripheral sympathetic ganglia GABA acts presynaptically to fa cilitate cholinergic transmission and postsynaptically to depolarize membra ne potential. The GABA effect on parasympathetic pancreatic ganglia is unkn own. We aimed to determine the effect of locally applied GABA on cat pancre atic ganglion neurons. Ganglia with attached nerve trunks were isolated fro m cat pancreata. Conventional intracellular recording techniques were used to record electrical responses from ganglion neurons. GABA pressure microej ection depolarized membrane potential with an amplitude of 17.4 +/- 0.7 mV. Electrically evoked fast excitatory postsynaptic potentials were significa ntly inhibited (5.4 +/- 0.3 to 2.9 +/- 0.2 mV) after GABA application. GABA -evoked depolarizations were mimicked by the GABA(A) receptor agonist musci mol and abolished by the GABA(A) receptor antagonist bicuculline and the Cl - channel blocker picrotoxin. GABA was taken up and stored in ganglia durin g preincubation with 1 mM GABA; beta -aminobutyric acid application after G ABA loading significantly (P< 0.05) increased depolarizing response to GABA (15.6 +/- 1.0 vs. 7.8 +/- 0.8 mV without GABA preincubation). Immunolabeli ng with antibodies to GABA, glial cell fibrillary acidic protein, protein g ene product 9.5, and glutamic acid decarboxylase (GAD) immunoreactivity sho wed that GABA was present in glial cells, but not in neurons, and that glia l cells did not contain GAD, whereas islet cells did. The data suggest that endogenous GABA released from ganglionic glial cells acts on pancreatic ga nglion neurons through GABA(A) receptors.