Neuroscience
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Using two-dimensional gel electrophoresis (2-DE), we examined proteomic changes in the caudal part of the spinal trigeminal nucleus induced by electrical stimulation of the dura mater surrounding the superior sagittal sinus (ES-SSS) in conscious rats. After image analysis of 2-DE gels, nine protein spots of interest were excised from the gels and identified by liquid chromatography-tandem mass spectrometry. ⋯ This result was validated with Real-time polymerase chain reaction and Western blot analyses. Because SSADH degrades GABA, decreased expression of it increases the local concentration of GABA in the caudal part of the spinal trigeminal nucleus after ES-SSS; this has not been reported before and may participate in the modulation of trigeminovascular headache.
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Estrogen receptors (ERs) α and β are involved in the regulation of the nitrergic system in the supraoptic (SON) and paraventricular (PVN) nuclei under basal conditions. In this study we have assessed whether ERs are also involved in the modulation of the nitrergic system in the SON and PVN under acute systemic hypertonic conditions. Adult ovariectomized rats received a single injection of either estradiol, a selective ERα agonist, a selective ERβ agonist, a selective ERα antagonist, a selective ERβ antagonist or vehicle. ⋯ In contrast, the inhibition of ERα enhanced the effect of NaCl, inducing a further decrease in the number of NADPH-diaphorase-positive cells. Moreover, the ERβ agonist enhanced and the ERβ antagonist blocked the effect of NaCl on the number of NADPH-diaphorase-positive neurons in the SON and in the medial magnocellular subdivision of the PVN. These findings indicate that estradiol regulates the nitrergic system in the SON and PVN under acute osmotic stress conditions, but the effects specifically depend on the anatomical subregions and different ERs.
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Cognitive dysfunction is relatively frequent in multiple sclerosis (MS) and it happens from the early stages of the disease. There is increasing evidence that the grey matter may be involved in autoimmune inflammation during relapses of MS. The purpose of this study was to evaluate if a single transfer of encephalitogenic T cells, mimicking a relapse of MS, may cause hippocampal damage and memory disturbances in rats. ⋯ The water maze test, however, did not reveal memory deficits. The present data indicate that a single transfer of autoimmune T cells results in preserved inflammation and probable on-going neuronal injury in the hippocampus, long after recovery from motor disturbances. These findings suggest that any relapse of the MS may start the neurodegenerative process in the hippocampus, which is not necessarily connected with memory deficits.
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Recent studies indicate that adiponectin can attenuate cerebral ischemic lesions via its functional area located in the C-terminal globular domain, which is called globular adiponectin (gAD). However, the mechanisms underlying this action remain unclear. In this study, we investigated the antioxidant properties of gAD during cerebral ischemia. ⋯ Furthermore, the activities of SOD and catalase increased, and the content of MDA reduced. However, TBCA blocked the effect of gAD on cerebral protection and its antioxidant abilities. Taken together, these results demonstrate that the neuroprotective action of gAD may result from the promotion of antioxidant capacity by inhibiting the NOX2 signaling system.
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To examine the effect of glucose on the cerebral metabolism of glutamine, rat brain slices were incubated with 5mM [3-(13)C]glutamine without and with 5mM unlabeled glucose. Tissue plus medium extracts were analyzed by using enzymatic and (13)C NMR techniques and fluxes through the enzymatic steps involved were calculated with a mathematical model. ⋯ The results indicate that 77% of the newly appeared glutamine was formed via glutamine synthetase and 23% from endogenous sources; the stimulation of [3-(13)C]glutamine removal by MSO also strongly suggests the existence of a cycle between [3-(13)C]glutamine and [3-(13)C]glutamate. This work also demonstrates that glucose increased fluxes through hexokinase, pyruvate kinase, lactate dehydrogenase, alanine aminotransferase, pyruvate carboxylase, pyruvate dehydrogenase, citrate synthase, flux from α-ketoglutarate to glutamate and flux through glutamine synthetase whereas it inhibited fluxes through aspartate aminotransferase, glutamic acid decarboxylase and GABA aminotransferase.