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Alcohol and Alcoholism Advance Access originally published online on July 9, 2009
Alcohol and Alcoholism 2009 44(5):443-448; doi:10.1093/alcalc/agp040
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© The Author 2009. Published by Oxford University Press on behalf of the Medical Council on Alcohol. All rights reserved

Role of the Endocannabinoid System in Ethanol-Induced Inhibition of Salivary Secretion

Juan Pablo Prestifilippo1,2*, Javier Fernández-Solari1,3, Vanina Medina4, Valeria Rettori3 and Juan Carlos Elverdin1

1 Cátedra de Fisiología, Facultad de Odontología, Universidad de Buenos Aires, Buenos Aires, Argentina
2 Cátedra de Fisiopatología, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina
3 Centro de Estudios Farmacológicos y Botánicos, Facultad de Medicina, Universidad de Buenos Aires (CEFyBO-CONICET-UBA), Buenos Aires, Argentina
4 Cátedra de Física, Laboratorio de Metodología de Radioisotopos, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina

* Corresponding author: Cátedra de Fisiología, Facultad de Odontología, Universidad de Buenos Aires, Marcelo T de Alvear 2142, piso 3, sector A Ciudad de Buenos Aires C1122, Argentina. Tel: +54-11-4964-1275; Fax: +54-11-4508-3958; E-mail: jprestifilippo{at}yahoo.com.ar

Received 16 March 2009; first review notified 30 April 2009; in revised form 27 May 2009, 31 May 2009 and 17 June 2009; accepted 18 June 2009; advance access publication 9 July 2009


  Abstract

Aim: The aim of the present study was to determine whether the endocannabinoid system could be involved in the ethanol-induced inhibition of salivation in adult male Wistar rats. Methods: Salivary secretion induced by different concentrations of methacholine, a cholinergic agonist, and the endocannabinoid arachidonoyl ethanolamide (anandamide, AEA) production in the submandibular gland (SMG) were determined in rats after ethanol (3 g/kg) administration by gastric gavage. To study the participation of cannabinod receptors in ethanol action, we evaluated methacholine-induced salivary secretion after ethanol administration when CB1 or CB2 receptors were blocked by intra-SMG injections of their selective antagonists AM251 and AM630, respectively. Additionally, we evaluated the in vitro effect of ethanol (0.1 M) on SMG production of cAMP, alone or combined with AM251 or AM630. Results: Acute ethanol administration increased AEA production in SMG and also inhibited the methacholine-induced saliva secretion that was partially restored by intraglandular injection of AM251 or AM630. In addition, ethanol significantly reduced the forskolin-induced increase in cAMP content in SMG in vitro while treatment with AM251 blocked this response. Conclusion: We conclude that the inhibitory effect produced by ethanol on submandibular gland salivary secretion is mediated, at least in part, by the endocannabinoid system.


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