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Background: Excessive exposure to club drug (GHB) would cause cognitive dysfunction in which impaired hippocampal Ca2+-mediated neuroplasticity may correlate with this deficiency. However, the potential changes of in vivo Ca2+ together with molecular machinery engaged in GHB-induced cognitive dysfunction has never been reported. Objective: This study aims to determine these changes in bioenergetic level through ionic imaging, spectrometric, biochemical, morphological, as well as behavioral approaches. Materials and methods: Adolescent rats subjected to GHB were processed for TOF-SIMS, immunohistochemistry, biochemical assay, together with Morris water maze to detect the ionic, molecular, neurochemical, and behavioral changes of GHB-induced cognitive dysfunction, respectively. Extent of oxidative stress and bio-energetics were assessed by levels of lipid peroxidation, Na+/K+ ATPase, cytochrome oxidase, and [14C]-2-deoxyglucose activity. Results: In GHB intoxicated rats, decreased Ca2+ imaging and reduced NMDAR1, nNOS, and p-CREB reactivities were detected in hippocampus. Depressed Ca2+-mediated signaling corresponded well with intense oxidative stress, diminished Na+/K+ ATPase, reduced COX, and decreased 2-DG activity, which all contributes to the development of cognitive deficiency. Conclusion: As impaired Ca2+-mediated signaling and oxidative stress significantly contribute to GHB-induced cognitive dysfunction, delivering agent (s) that improves hippocampal bio-energetics may thus serve as a promising strategy to counteract the club druginduced cognitive dysfunction emerging in our society …
Publication date: 
1 Jan 2015

F Faure, S Díaz, T Araneda, M Taub, M Millán, A Hoffmann, F Bustos, A Barros, D González, R Fritsch

Biblio References: 
Volume: 357 Pages: e215-e234
Abstracts/Journal of the Neurological Sciences