Acetate as an active metabolite of ethanol: studies of locomotion, loss of righting reflex, and anxiety in rodents
View/ Open
Impact
Scholar |
Other documents of the author: Pardo Andrés, Marta; Betz, Adrienne J.; San Miguel Segura, Noemí; López Cruz, Laura; Salamone, John; Correa, Merce
Metadata
Show full item recordcomunitat-uji-handle:10234/9
comunitat-uji-handle2:10234/8033
comunitat-uji-handle3:10234/8636
comunitat-uji-handle4:
INVESTIGACIONMetadata
Title
Acetate as an active metabolite of ethanol: studies of locomotion, loss of righting reflex, and anxiety in rodentsAuthor (s)
Date
2013Publisher
FrontiersISSN
1662-5153Bibliographic citation
Front Behav Neurosci. 2013; 7: 81.Type
info:eu-repo/semantics/articlePublisher version
http://journal.frontiersin.org/Journal/10.3389/fnbeh.2013.00081/abstractSubject
Abstract
It has been postulated that a number of the central effects of ethanol are mediated via ethanol metabolites: acetaldehyde and acetate. Ethanol is known to produce a large variety of behavioral actions such anxiolysis, ... [+]
It has been postulated that a number of the central effects of ethanol are mediated via ethanol metabolites: acetaldehyde and acetate. Ethanol is known to produce a large variety of behavioral actions such anxiolysis, narcosis, and modulation of locomotion. Acetaldehyde contributes to some of those effects although the contribution of acetate is less known. In the present studies, rats and mice were used to assess the acute and chronic effects of acetate after central or peripheral administration. Male Sprague-Dawley rats were used for the comparison between central (intraventricular, ICV) and peripheral (intraperitoneal, IP) administration of acute doses of acetate on locomotion. CD1 male mice were used to study acute IP effects of acetate on locomotion, and also the effects of chronic oral consumption of acetate (0, 500, or 1000 mg/l, during 7, 15, 30, or 60 days) on ethanol- (1.0, 2.0, 4.0, or 4.5 g/kg, IP) induced locomotion, anxiolysis, and loss of righting reflex (LORR). In rats, ICV acetate (0.7–2.8 μmoles) reduced spontaneous locomotion at doses that, in the case of ethanol and acetaldehyde, had previously been shown to stimulate locomotion. Peripheral acute administration of acetate also suppressed locomotion in rats (25–100 mg/kg), but not in mice. In addition, although chronic administration of acetate during 15 days did not have an effect on spontaneous locomotion in an open field, it blocked ethanol-induced locomotion. However, ethanol-induced anxiolysis was not affected by chronic administration of acetate. Chronic consumption of acetate (up to 60 days) did not have an effect on latency to, or duration of LORR induced by ethanol, but significantly increased the number of mice that did not achieve LORR. The present work provides new evidence supporting the hypothesis that acetate should be considered a centrally-active metabolite of ethanol that contributes to some behavioral effects of this alcohol, such as motor suppression. [-]
Is part of
Frontiers in Behavioral Neuroscience, 2013, vol. 7, no 81Rights
© 2007 - 2014 Frontiers Media S.A. All Rights Reserved. This Document is Protected by copyright and was first published by Frontiers. All rights reserved. it is reproduced with permission.
http://rightsstatements.org/vocab/InC/1.0/
info:eu-repo/semantics/openAccess
http://rightsstatements.org/vocab/InC/1.0/
info:eu-repo/semantics/openAccess
This item appears in the folowing collection(s)
- PSB_Articles [1293]