Transmitter and electrical stimulations of [3H]taurine release from rat sympathetic ganglia.

Astroglial cells release taurine in response to stimulation with neurotransmitters. This process has been studied most extensively with primary cultures of astrocytes and LRM55 glial cells. These studies have demonstrated that several transmitters can elicit release. The second messenger systems involved in activating release have been characterized (10, 15, 19). An important issue concerning all studies of this type is the applicability of results obtained with glia in culture to glia in vivo. We have chosen the rat superior cervical ganglion as a nervous tissue having the potential for exploring taurine release from glial cells in situ. The major neuronal composition of the ganglion consists of preganglionic nerve terminals providing cholinergic input and principal neurons providing noradrenergic output. The superior cervical ganglion also contains a very small population of dopamine-containing intrinsic neurons known as SIF cells (3). The glial population of the superior cervical ganglion is composed of Schwann cells responsible for myelination and satellite glia, immunoreactive to glial fibrillary acidic protein, that surround the cell bodies of the principal neurons (1, 7). Currently available data suggest that taurine is selectively taken up by the satellite glia. Autoradiographic studies have demonstrated that the ω-amino acids GABA and β-alanine are selectively accumulated by satellite glial cells in the superior cervical ganglion (5, 20), while transport studies have shown that taurine inhibits [3H]GABA uptake and that GABA inhibits [14C]taurine uptake by the superior cervical ganglion (5). The demonstration that potassium-stimulated efflux of [3H]GABA from the superior cervical ganglion is not reduced by preganglionic denervation also supports the glial localization of ω-amino acid transporters in this tissue (4).