Neuronal and Glial Release of [3H]GABA from the Rat Olfactory Bulb

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Abstract
Neuronal vs. glial components of [3H]GABA release were studied in 2 different microdissected layers of the olfactory bulb of the rat: the olfactory nerve layer (ONL), consisting mainly of glial cells, and the external plexiform layer (EPL) with a high density of GABAergic dendritic terminals. In some experiments substantia nigra was used as a GABAergic axonal system and the trigeminal ganglia as a peripheral glial model. Spontaneous release of [3H]GABA was always lower in neuronal elements compared with glial cells. A veratridine-evoked release was observed from the ONL but not from the trigeminal ganglia. Tetrodotoxin abolished the veratridine-evoked release from the ONL, which also showed partial inhibition when high Mg concentrations were used in a Ca2+-free solution. .beta.-Alanine was strongly exchanged with [3H]GABA from the ONL of animals with the olfactory nerve lesioned and from animals with no lesion, but only a small heteroexchange was found from the external plexiform layer. The .beta.-alanine heteroexchange was able to deplete the releasable GABA store from the ONL of lesioned animals. In nonlesioned animals and the EPL, veratridine-stimulated release of [3H]GABA was not significantly reduced after the .beta.-alanine heteroexchange. Stimulation of the [3H]GABA release by high concentrations of K+ elicited a higher release rate from axonal terminals than from dendrites or glia. Neurons and glia showed a similar inhibition of [3H]GABA release when a high Mg concentration was added to a Ca-free solution. When D-600 [.alpha.-isopropyl-.alpha.-(N-methyl-N-homoveratryl-.gamma.-aminopropyl)-3,4,5-trimethoxyphenylacetonitrile] was used as a Ca-flux blocker, no inhibition of the release was observed in glial cells, whereas an almost complete blockage was found in both neuronal preparations (substantia nigra and EPL). The results provide further evidence for differential release mechanisms of GABA from CNS neurons and glial cells.