In:
Scientific Reports, Springer Science and Business Media LLC, Vol. 5, No. 1 ( 2015-12-17)
Abstract:
Excessive exposure to club drug (GHB) would cause cognitive dysfunction in which impaired hippocampal Ca 2+ -mediated neuroplasticity may correlate with this deficiency. However, the potential changes of in vivo Ca 2+ together with molecular machinery engaged in GHB-induced cognitive dysfunction has never been reported. This study aims to determine these changes in bio-energetic level through ionic imaging, spectrometric, biochemical, morphological, as well as behavioral approaches. 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 [ 14 C]-2-deoxyglucose activity. Results indicated that in GHB intoxicated rats, decreased Ca 2+ imaging and reduced NMDAR1, nNOS and p-CREB reactivities were detected in hippocampus. Depressed Ca 2+ -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. As impaired Ca 2+ -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 drug-induced cognitive dysfunction emerging in our society nowadays.
Type of Medium:
Online Resource
ISSN:
2045-2322
Language:
English
Publisher:
Springer Science and Business Media LLC
Publication Date:
2015
detail.hit.zdb_id:
2615211-3
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