NDLI: Cross-regulation between colocalized nicotinic acetylcholine and $5-HT_{3}$ serotonin receptors on presynaptic nerve terminals

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Cross-regulation between colocalized nicotinic acetylcholine and $5-HT_{3}$ serotonin receptors on presynaptic nerve terminals

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Dougherty, John J. Nichols, Robert A.
Description	Country affiliation: United States Author Affiliation: Dougherty JJ ( Department of Pharmacology & Physiology, Drexel University College of Medicine, Philadelphia, PA 19102, USA.)
Abstract	Aim: Substantial colocalization of functionally independent α4 nicotinic acetylcholine receptors and $5-HT_{3}$ serotonin receptors on presynaptic terminals has been observed in brain. The present study was aimed at addressing whether nicotinic acetylcholine receptors and $5-HT_{3}$ serotonin receptors interact on the same presynaptic terminal, suggesting a convergence of cholinergic and serotonergic regulation. Methods: $Ca^{2+}$ responses in individual, isolated nerve endings purified from rat striatum were measured using confocal imaging. Results: Application of 500 nmol/L nicotine following sustained stimulation with the highly selective $5-HT_{3}$ receptor agonist m-chlorophenylbiguanide at 100 nmol/L resulted in markedly reduced $Ca^{2+}$ responses (28% of control) in only those striatal nerve endings that originally responded to m-chlorophenylbiguanide. The cross-regulation developed over several minutes. Presynaptic nerve endings that had not responded to m-chlorophenylbiguanide, indicating that $5-HT_{3}$ receptors were not present, displayed typical responses to nicotine. Application of m-chlorophenylbiguanide following sustained stimulation with nicotine resulted in partially attenuated $Ca^{2+}$ responses (49% of control). Application of m-chlorophenylbiguanide following sustained stimulation with m-chlorophenylbiguanide also resulted in a strong attenuation of $Ca^{2+}$ responses (12% of control), whereas nicotine-induced $Ca^{2+}$ responses following sustained stimulation with nicotine were not significantly different from control. Conclusion: These results indicate that the presynaptic $Ca^{2+}$ increases evoked by either $5-HT_{3}$ receptor or nicotinic acetylcholine receptor activation regulate subsequent responses to $5-HT_{3}$ receptor activation, but that only $5-HT_{3}$ receptors cross-regulate subsequent nicotinic acetylcholine receptor-mediated responses. The findings suggest a specific interaction between the two receptor systems in the same striatal nerve terminal, likely involving $Ca^{2+}-dependent$ intracellular pathways that regulate these signaling systems at one or more levels.
File Format	HTM / HTML
ISSN	16714083
e-ISSN	17457254
DOI	10.1038/aps.2009.62
Journal	Acta Pharmacologica Sinica
Issue Number	6
Volume Number	30
Language	English
Publisher	Macmillan Publishers Limited
Publisher Date	2009-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Pharmacology Calcium Metabolism Presynaptic Terminals Receptors, Nicotinic Receptors, Serotonin, 5-ht3 Animals Biguanides Pharmacology Corpus Striatum Microscopy, Confocal Nicotine Nicotinic Agonists Drug Effects Rats, Sprague-dawley Serotonin Receptor Agonists Signal Transduction Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Pharmacology Pharmacology (medical)

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