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 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 Ca(2+) as the mechanism involved in the neurobehavioral effects elicited by EtOH.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Tarragon E,Baliño P,Aragon CMdoi
10.1016/j.neulet.2014.07.046subject
Has Abstractpub_date
2014-09-19 00:00:00pages
68-73eissn
0304-3940issn
1872-7972pii
S0304-3940(14)00627-2journal_volume
580pub_type
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