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Objective(s): Nowadays, the electromagnetic field-emitting devices are used routinely in our lives. Controversial reports exist concerning the effects of mobile radiofrequency (RF) on different parts of the body, especially stress hormones. The main goal of the present work was to study the long-term effects of mobile RF900 MHz exposure with special focus on the adrenal gland pathophysiology and function. Materials and Methods: Adult male Wistar rats were exposed to mobile RF 6 hr daily for 4-8 weeks. Intact and switched-off exposed animals were considered as controls. Plasma ACTH and cortisol levels were measured by the ELISA method. At the end of the experiment, a histological study was done on adrenal gland and brain tissues by hematoxylin and eosin staining. The thickness of the fasciculate layer of the adrenal gland, and its cell count and perimeter were measured using the Fiji software. Results: Enhanced plasma ACTH and cortisol levels were found after prolonged exposure to mobile RF. The fasciculata layer of adrenal cortex eventually thickened following mobile RF radiation. While the number of cells in zona fasciculata remained constant, the cell size and perimeter increased during RF exposure. Finally, we found that vacuolization in brain tissue and the number and size of vacuoles considerably increased during two months of RF exposure. Conclusion: Cell phone RF exposure induced significant hormonal and structural changes in adrenal gland and brain tissues. Therefore, the public should be aware and limit their exposure as much as possible. [ABSTRACT FROM AUTHOR]

Introduction: Synaptosomes are sealed particles that contain mitochondria, cytoskeleton and vesicles which are necessary to synaptic events like neurotransmitter release and uptake in the nervous system. However, the effect of high and low temperatures on synaptosome membrane integrity and function during a time course after its extraction is less known. The purpose of this study was to assess synaptosome viability and function at 37, 4°C and room temperature (RT) during 6 hours after its extraction. Methods: Hippocampi of 40 male Wistar rats were used for synaptosome preparation. To ensure synaptosome membrane integrity and function, lactate dehydrogenase activity (LDH) and GABA uptake were assessed during 6 successive hours after their extraction at 37, 4°C and RT. Results: Our results showed that at 37°C, synaptosome membrane integrity was reduced 3 hours but at 4°C and RT, it occurred 5 hours following their extraction. The results of synaptosome function analysis coincide with LDH enzyme assay data, meaning that GABA uptake faced a 50% reduction from the initial value at 37°C after 3 hours and at RT after 5 hours. We also found that GABA uptake was reduced at 4°C in the first hour after extraction because the low temperature inhibits GABA transporters. Conclusion: Synaptosomes preserved their viability and function at RT, 37 and 4°C at least for 3 hours after extraction and reduced over time. For long term application of synaptosomes, it is better to keep them at 4°C. [ABSTRACT FROM AUTHOR]

Introduction: Recently, herbal medicine is widely used as an alternative and complementary therapy in several neurological disorders such as epilepsy. The anti-inflammatory and neuroprotective effects of Zingiber officinale or ginger have been well-documented. The present study was designed to evaluate the effects of ginger extract pre-treatment on seizures behavior, neuronal density and astrocytes activation in pentylenetetrazol (PTZ)- induced kindling model. Methods: Kindling model was induced in mice by repetitive administration of PTZ at sub convulsive dose. Hydroalcoholic extract of ginger at doses of 25, 50 or 100 mg/kg were daily injected 10 days before PTZ injections and intraperitoneal administration of extract was continued 1h before each PTZ injection. Immunostaining against NeuN and GFAP as neuronal and astrocyte markers, respectively, was carried out on brain tissue sections. Results: Our data showed that ginger extract pre-treatment, especially at dose of 100 mg/kg, reduced the seizures behavior in PTZ receiving animals. Immunostaining against NeuN biomarker demonstrated that neuronal death was alleviated in animals under treatment of ginger extract. Furthermore, application of ginger extract attenuated the number of GFAP expressing cells in hippocampus of fully-kindled animals. Conclusion: Overall, our data suggest that ginger pre-treatment exerts significant neuroprotective effect by attenuation of astrocytes activation in PTZ-induced kindling model. It can be concluded that ginger might be used as effective supplementary agent in epileptic patients. [ABSTRACT FROM AUTHOR]

Introduction: Nogo-A and Nogo receptor (NgR) are expressed in the subventricular zone (SVZ) stem cells. NgR plays critical inhibitory roles in axonal regeneration and remyelination. However, the role of NgR in SVZ niche behaviors in demyelination context is still uncertain. Here we investigated the effects of NgR inhibition on SVZ niche reaction in a local model of demyelination in adult mouse optic chiasm. Methods: Demyelination was induced in adult mouse optic chiasm by microinjection of lysolecithin. We injected siRNAs against NgR intracerebroventricularly via a permanent cannula over 14 days to knockdown NgR. To trace SVZ stem cells and assess the effect of NgR inhibition on their reaction, BrdU was injected to the animals prior to the demyelination induction. Immunohistochemistry and histological analysis was carried out 3, 7 and 14 days post demyelination lesion. Results: NgR inhibition significantly increased the numbers of proliferating cells in SVZ in response to demeylination. The number of BrdU+/Olig2+progenitor cells in the neurogenic zone of the lateral ventricles was enhanced when NgR was blocked. These progenitor cells (Olig2+, GFAP+ or PSA-NCAM) were mobilized away from this SVZ as a function of time. Inhibition of NgR significantly reduced demyelination extension in optic chiasm. Conclusion: Our findings reveal that inhibition of NgR potentiates adult SVZ progenitor cells proliferation and differentiation in demyelination condition and facilitates remyelination in the optic chiasm. Therefore, inhibition of NgR function could have therapeutic potential for demyelinating disease like multiple sclerosis. [ABSTRACT FROM AUTHOR]

Objective: Glioblastoma (GBM) is the most malignant and aggressive type of glioma, associated with a high rate of mortality. The transforming growth factor-β receptor II (TGFβ RII) is involved in glioma initiation and progression. On the other hand, TGFβ RII silencing is critical to the inhibition of GBM. Therefore, we aimed to determine the effects of specific TGFβ RII siRNA on the survival of U-373MG cells. Methods: TGFβ RII siRNA was transfected, and qRT-PCR was performed to examine TGFβ RII mRNA expression. Cell survival was determined using colorimetric MTT assay, and platelet-derived growth factor-BB (PDGF-BB) level was measured in the culture supernatant using ELISA assay. Result: Our findings indicated that specific siRNAs could dose-dependently suppress TGFβ RII mRNA expression after 48 hours. In addition, treatment with TGFβ RII siRNA significantly reduced tumor cell survival and decreased the amount of PDGF-BB protein in the cell culture supernatant. Conclusion: Our results suggest that TGFβ RII silencing can be a promising complementary treatment for glioma., (Creative Commons Attribution License)