GABAergic Action on Cholinergic Axon Terminals in the Superior Cervical Ganglion

Abstract

Interactions between different neuronal or transmitter systems are considered to play an important role in the regulation of the function of the mammalian sympathetic ganglia. The excitatory effect of acetylcholine (ACh) in the superior cervical ganglia (SCG) has been well documented by electrophysiological techniques [18, 27, 35, 37]. The elements of the ACh system (choline acetyltransferase, ChAT [4, 7, 14, 22, 29, 39, 42]; ACh [10, 36]; acetylcholinesterase, AChE [24, 28, 29, 46]; muscarinic acetylcholine receptor, mAChR [8, 9, 26, 34, 41]; nicotinic acetylcholine receptor, nAChR [20, 21, 25, 38]) have also been demonstrated. Other neurotransmitters, such as γ-aminobutyric acid (GABA), are known to effect synaptic transmission between preganglionic axon terminals and postganglionic sympathetic neurons [1, 5, 11, 16, 23]. More recently, an immunocytochemical technique [13] was used to demonstrate GABA-positive fibers [12, 31, 45] and GABA-positive cells [44] in the SCG. What is the morphological basis of the GABAergic interaction with cholinergic nerve fibers? How does GABA affect the release of ACh from cholinergic axon terminals? What kind of GABA receptors play a role in the GABAergiccholinergic interaction? These questions are addressed in the present paper.