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Vol. 280, Issue 2, 650-655, 1997

Positive Feedback Modulation of Acetylcholine Release from Isolated Rat Superior Cervical Ganglion1

Shang-Dong Liang2 and E. Sylvester Vizi

Department of Pharmacology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary

The effects of selective nicotinic acetylcholine (ACh) receptor (nAChR) agonists and antagonists on the stimulation-evoked release of [3H]ACh were studied in rat isolated superior cervical ganglion loaded with [3H]choline and superfused in a 2-ml chamber. Nicotine and 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP), but not cytisine, increased the stimulation (2 Hz)-evoked release of [3H]ACh in a concentration-dependent manner. The rank order of potency to increase stimulation-evoked release for the nAChR agonists (nicotine > DMPP >>  cytisine) suggests that the beta 4 subunit of nAChRs is not involved in the release. The finding that alpha -bungarotoxin was effective in preventing the effect of DMPP and itself significantly reduced the release indicates that the alpha 7 subunit is located presynaptically and may be involved in the positive feedback modulation. Hexamethonium inhibited the effect of DMPP with an apparent dissociation constant (Kd) of 11.5 ± 1.5 µM. Hexamethonium and other nAChR antagonists, i.e., (+)-tubocurarine (100 µM), mecamylamine (3 µM), dihydro-beta -erythroidine (3 µM), pancuronium (10 µM) and alpha -bungarotoxin (2 µM), also decreased the stimulation-evoked release of [3H]ACh. The effect of hexamethonium was independent of stimulation frequency (2, 10 and 30 Hz) applied. Atropine enhanced the stimulation-evoked release of ACh, indicating that there is negative feedback modulation of ACh release associated with neuronal activity. In contrast, when the nicotinic positive feedback was prevented by hexamethonium, atropine failed to enhance the release. These findings indicate that muscarinic receptor-mediated inhibition of ACh release functions in cases in which the release is enhanced by ACh via stimulation of presynaptic nAChRs. A similar interaction was found between A1 receptor-mediated reduction and nAChR-mediated positive feedback modulation of [3H]ACh release. The results suggest the presence of positive feedback modulation of ACh release via presynaptic nAChRs in rat superior cervical ganglion.

Copyright © by The American Society for Pharmacology and Experimental Therapeutics


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