Post-traumatic stress disorder in adults victims of fire in Valparaiso, Chile, April 2014

Abstract

Background: 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. 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 [ 14 C]-2-deoxyglucose activity. Results: 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. Conclusion: 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 druginduced cognitive dysfunction emerging in our society nowadays.