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Objective: Epilepsy is accompanied by inflammation, and the anti-inflammatory agents may have anti-seizure effects. In this investigation, the effect of deep brain stimulation, as a potential therapeutic approach in epileptic patients, was investigated on seizure-induced inflammatory factors. Materials and Methods: In the present experimental study, rats were kindled by chronic administration of pentylenetetrazol (PTZ; 34 mg/Kg). The animals were divided into intact, sham, low-frequency deep brain stimulation (LFS), kindled, and kindled +LFS groups. In kindled+LFS and LFS groups, animals received four trains of intra-hippocampal low-frequency deep brain stimulation (LFS) at 20 minutes, 6, 24, and 30 hours after the last PTZ injection. Each train of LFS contained 200 pulses at 1 Hz, 200 µA, and 0.1 ms pulse width. One week after the last PTZ injection, the Y-maze test was run, and then the rats’ brains were removed, and hippocampal samples were extracted for molecular assessments. The gene expression of two pro-inflammatory factors [interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α)], and glial fibrillary acidic protein (GFAP) immunoreactivity (as a biological marker of astrocytes reactivation) were evaluated. Results: Obtained results showed a significant increase in the expression of of interleukin-6 (IL-6), tumor necrosis factor (TNF)-α, and GFAP at one-week post kindling seizures. The application of LFS had a long-lasting effect and restored all of the measured changes toward normal values. These effects were gone along with the LFS improving the effect on working memory in kindled animals. Conclusion: The anti-inflammatory action of LFS may have a role in its long-lasting improving effects on seizure-induced cognitive disorders. [ABSTRACT FROM AUTHOR]

Abstract: The hippocampus is essentially involved in learning and memory, and is known to be a target for androgen actions. As neuron–astrocyte interactions play a crucial role during development and in the adult brain, it is thought that astrocytes support learning and memory through specific mechanisms. In this study, the effect of testosterone-induced impairment of acquisition and retrieval of long-term memory, on the number of astrocytes was studied. Adult male albino Wistar rats were bilaterally cannulated into the CA1 region and received 80μg/0.5μl of testosterone enanthate dissolved in DMSO as vehicle. In trained groups injection was done 30min before training. Our results showed that pre-training administration of testosterone increased escape latency and the traveled distance, as compared to intact or DMSO administered (sham-operated) counterparts. Testosterone administration also increased the number of astrocytes in rats, compared to sham-operated and intact animals in both trained and non-trained groups. We have also found that spatial learning could increase the number of astrocytes in the hippocampus as a center of long-term learning and memory and recall. It is concluded that, testosterone-induced impairment in learning and memory, causes an increase in the number of astrocytes in the CA1 region of rat hippocampus. [Copyright &y& Elsevier]

• THC administration interrupts long term memory and long term potentiation. • Stereological studies revealed considerable atrophy in hippocampus. • Several signaling cascades related to synaptic regulation were interrupted in hippocampus under THC administration. Tetrahydrocannabinol (THC), a major psychoactive constituent of marijuana, can substantially change the function of several brain areas, leading to behavioral impairment including memory and learning dysfunction. Given the importance of hippocampus as one of the chief parts of the brain involved in memory processing, the present study seeks to investigate structural and histological alterations in hippocampus as well as behavioral defects provoked by THC treatment. Besides, using genome-wide sequencing, we adopted a pathway-based approach to discover dysregulated molecular pathways. Our results demonstrated remarkable hippocampal atrophy, and also interrupted memory function and long term potentiation (LTP) under THC exposure. We also detected several dysregulated signaling pathways involved in synaptic plasticity as well as cell-cell interaction in the hippocampus of THC-treated rats. Overall, the results indicate a potential correlation between disrupted signaling cascades, hippocampal atrophy and memory defects caused by THC treatment. [ABSTRACT FROM AUTHOR]