• J M Hills, B F King, R Mirsky, and K R Jessen.
• Smith, Kline and French Research, Welwyn, Hertfordshire, U.K.
• J. Auton. Nerv. Syst. 1988 Mar 1; 22 (2): 129-40.

AbstractImmunohistochemical techniques were used to detect the presence of a GABA-like material in prevertebral sympathetic ganglia in guinea-pigs. Varicose, immunolabelled nerve fibres were observed in close proximity to sympathetic neurones in inferior mesenteric ganglia and coeliac ganglia. Non-varicose, immunolabelled nerve fibres were observed in lumbar colonic nerves and superior coeliac nerves, i.e. in nerve bundles peripheral to prevertebral ganglia. Immunolabelling was also present in neurones in the myenteric plexus and in nerve fibres in the circular muscle of the colon, as shown previously (Hills et al., Neuroscience, 22 (1987) 301-312). However, GABA-like immunoreactivity was not observed in the cell bodies of prevertebral ganglia nor in splanchnic nerves central to prevertebral ganglia. It was concluded from these results that prevertebral ganglia in guinea-pig receive a GABAergic innervation from neurones peripheral to the ganglia, possibly from GABA-containing neurones in the myenteric plexus of the gastrointestinal tract. Intracellular recordings were made from sympathetic neurones in the inferior mesenteric ganglion (IMG). Application of GABA onto the IMG caused a slow depolarisation of sympathetic neurones, during which there was a marked decrease in the input resistance of IMG cells. Application of GABA also depressed excitatory postsynaptic potentials (EPSPs) and action potentials in sympathetic neurones excited by cholinergic nerve fibres in the lumbar colonic nerves. The reversal potential of the GABA-induced slow depolarisation was -37 mV, a value close to the chloride equilibrium potential for sympathetic neurones. The actions of GABA were reversibly reduced by the GABAA antagonist, bicuculline, and were modulated in a predictable manner by substituting chloride ions with methane-sulphonate ions. These results indicated that GABA, and presumably GABAergic nerves in prevertebral ganglia, modulate the excitability of sympathetic neurones by acting on GABAA receptors linked to a chloride ionophore.

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