Summary
The possible involvement of GABAergic mechanisms in the catecholamine (CA) release from adrenal medulla was investigated in a primary culture of bovine adrenal chromaffin cells. GABA elicited CA release and enhanced acetylcholine (ACh)-, excess K+-and veratridine-evoked CA release. Muscimol, a selective GABAA receptor agonist, mimicked the action of GABA on CA release. On the other hand, baclofen, a GABAB receptor agonist, failed to affect basal or evoked CA release. Furthermore, bicuculline and picrotoxin blocked the enhancement by GABA of veratridine-evoked CA release without affecting basal CA release and CA release evoked by veratridine. In Ca2+-free medium, GABA failed to affect basal and caffeine-evoked CA release. ACh-evoked CA release was slightly reduced by bicuculline, whereas excess K+-evoked CA release was not, suggesting the involvement of endogenous GABA in CA release evoked by ACh. These results suggest a facilitatory modulation by GABA of basal and evoked release of CA from bovine adrenal medulla through GABAA receptor-mediated mechanisms.
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Kitayama, S., Morita, K., Dohi, T. et al. Enhancement by GABA of the stimulation-evoked catecholamine release from cultured bovine adrenal chromaffin cells. Naunyn-Schmiedeberg's Arch Pharmacol 341, 414–418 (1990). https://doi.org/10.1007/BF00176333
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DOI: https://doi.org/10.1007/BF00176333