Time and Brain Region-Dependent Excitatory Neurochemical Alterations in Bilateral Common Carotid Artery Occlusion Global Ischemia Model.

Strict metabolic regulation in discrete brain regions leads to neurochemical changes in cerebral ischemia. Accumulation of extracellular glutamate is one of the early neurochemical changes that take place during cerebral ischemia. Understanding the sequential neurochemical processes involved in cerebral ischemia-mediated excitotoxicity before the clinical intervention of revascularization and reperfusion may greatly influence future therapeutic strategies for clinical stroke recovery. This study investigated the influence of time and brain regions on excitatory neurochemical indices in the bilateral common carotid artery occlusion (BCCAO) model of global ischemia. Male Wistar rats were subjected to BCCAO for 15 and 60 min to evaluate the effect of ischemia duration on excitatory neurochemical indices (dopamine level, glutamine synthetase, glutaminase, glutamate dehydrogenase, aspartate aminotransferase, monoamine oxidase, acetylcholinesterase, and Na+ K+ ATPase activities) in the discrete brain regions (cortex, striatum, cerebellum, and hippocampus). BCCAO without reperfusion caused marked time and brain region-dependent alterations in glutamatergic, glutaminergic, dopaminergic, monoaminergic, cholinergic, and electrogenic homeostasis. Prolonged BCCAO decreased cortical, striatal, and cerebellar glutamatergic, glutaminergic, dopaminergic, cholinergic, and electrogenic activities; increased hippocampal glutamatergic, glutaminergic, dopaminergic, and cholinergic activities, increased cortical and striatal monoaminergic activity; decreased cerebellar and hippocampal monoaminergic activity; and decreased hippocampal electrogenic activity. This suggests that excitatory neurotransmitters play a major role in the tissue-specific metabolic plasticity and reprogramming that takes place between the onset of cardiac arrest-mediated global ischemia and clinical intervention of recanalization. These tissue-specific neurochemical indices may serve as diagnostic and therapeutic strategies for mitigating the progression of ischemic damage before revascularization.

Effect of mobile phone radiation on oxidative stress, inflammatory response, and contextual fear memory in Wistar rat.

In the present lifestyle, we are continuously exposed to radiofrequency electromagnetic field (RF-EMF) radiation generated mainly by mobile phones (MP). Among other organs, our brain and hippocampus in specific, is the region where effect of any environmental perturbation is most pronounced. So, this study was aimed to examine changes in major parameters (oxidative stress, level of pro-inflammatory cytokines (PICs), hypothalamic-pituitary-adrenal (HPA) axis hormones, and contextual fear conditioning) which are linked to hippocampus directly or indirectly, upon exposure to mobile phone radiofrequency electromagnetic field (MP-RF-EMF) radiation. Exposure was performed on young adult male Wistar rats for 16 weeks continuously (2 h/day) with MP-RF-EMF radiation having frequency, power density, and specific absorption rate (SAR) of 1966.1 MHz, 4.0 mW/cm2, and 0.36 W/kg, respectively. Another set of animals kept in similar conditions without any radiation exposure serves as control. Towards the end of exposure period, animals were tested for fear memory and then euthanized to measure hippocampal oxidative stress, level of circulatory PICs, and stress hormones. We observed significant increase in hippocampal oxidative stress (p < 0.05) and elevated level of circulatory PICs viz. IL-1beta (p < 0.01), IL-6 (p < 0.05), and TNF-alpha (p < 0.001) in experimental animals upon exposure to MP-RF-EMF radiation. Adrenal gland weight (p < 0.001) and level of stress hormones viz. adrenocorticotropic hormone (ACTH) (p < 0.01) and corticosterone (CORT) (p < 0.05) were also found to increase significantly in MP-RF-EMF radiation-exposed animals as compared with control. However, alteration in contextual fear memory was not significant enough. In conclusion, current study shows that chronic exposure to MP-RF-EMF radiation emitted from mobile phones may induce oxidative stress, inflammatory response, and HPA axis deregulation. However, changes in hippocampal functionality depend on the complex interplay of several opposing factors that got affected upon MP-RF-EMF exposure.