gamma-Aminobutyric acid-induced modulation of acetylcholine release from the guinea pig lung.
gamma-Aminobutyric acid (GABA) content was measured biochemically and the effect of GABA on the release of [3H]acetylcholine (ACh) was studied in strips of the guinea pig lung preloaded with [3H]choline. GABA contents were highest in the middle sections of the lung, as compared with proximal and distal areas. GABA evoked the release of [3H]ACh from the strips of the lung. The effect of GABA was mimicked by muscimol and antagonized by bicuculline and furosemide. Perfusion with Ca++-free medium and tetrodotoxin, but not nipecotic acid, inhibited the GABA- and muscimol-evoked release of [3H]ACh, thereby indicating that the released ACh was of neuronal origin. Diazepam and pentobarbital potentiated the muscimol-evoked [3H]ACh release. On the other hand, GABA reduced the KCl (40 mM)-evoked release of [3H]ACh in the presence of tetrodotoxin and bicuculline and baclofen mimicked the inhibitory effect of GABA. The effects of GABA and baclofen were not altered by alpha and beta adrenergic antagonists. These findings provide evidence for two types of GABA receptors in the lung of the guinea pig, and these receptors are involved in regulating the release of ACh.[1]References
- gamma-Aminobutyric acid-induced modulation of acetylcholine release from the guinea pig lung. Shirakawa, J., Taniyama, K., Tanaka, C. J. Pharmacol. Exp. Ther. (1987) [Pubmed]
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