Centrally formed acetaldehyde mediates ethanol-induced brain PKA activation
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Other documents of the author: Tarragon Cros, Ernesto; Baliño, Pablo; González Aragón, Carlos Manuel
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comunitat-uji-handle2:10234/8033
comunitat-uji-handle3:10234/8636
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Title
Centrally formed acetaldehyde mediates ethanol-induced brain PKA activationDate
2014Publisher
ElsevierISSN
0304-3940; 1872-7972Bibliographic citation
TARRAGON, E.; BALIÑO, P.; GONZÁLEZ ARAGÓN, C. M. Centrally formed acetaldehyde mediates ethanol-induced brain PKA activation. Neuroscience letters, 2014, vol. 580, p. 68-73.Type
info:eu-repo/semantics/articlePublisher version
http://www.sciencedirect.com/science/article/pii/S0304394014006272Version
info:eu-repo/semantics/submittedVersionSubject
Abstract
Centrally formed acetaldehyde has proven to be responsible for several psychopharmacological effects induced by ethanol. In addition, it has been suggested that the cAMP-PKA signaling transduction pathway plays an ... [+]
Centrally formed acetaldehyde has proven to be responsible for several psychopharmacological effects induced by ethanol. In addition, it has been suggested that the cAMP-PKA signaling transduction pathway plays an important role in the modulation of several ethanol-induced behaviors. Therefore, we hypothesized that acetaldehyde might be ultimately responsible for the activation of this intracellular pathway. We used three pharmacological agents that modify acetaldehyde activity (α-lipoic acid, aminotriazole, and d-penicillamine) to study the role of this metabolite on EtOH-induced PKA activation in mice. Our results show that the injection of α-lipoic acid, aminotriazole and d-penicillamine prior to acute EtOH administration effectively blocks the PKA-enhanced response to EtOH in the brain. These results strongly support the hypothesis of a selective release of acetaldehyde-dependent Ca2+ as the mechanism involved in the neurobehavioral effects elicited by EtOH. [-]
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Neuroscience letters, 2014, vol. 580Rights
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