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Objective To study the effects of mild hypothermia on cognitive function , synapsinⅠexpression and synaptic ultrastructure of hippocampus in epileptic rats induced by global cerebral ischemia. Methods Forty-eight male SD rats were randomly divided into control (NC) group, sham-operated (Sham) group, normothermic epilepsy (NT) group and mild hypothermic epilepsy (HT) group. The model of postischemic audio-genetic seizure was established by chest compression. Hypothermia intervention was given to HT group. Immunocytochemistry was conducted to detect the expressions of synapsin I in hippocampus at days 1 , 3, 14. the synaptic ultrastructure and cognitive function were respectively observed by electron microscope and Morris water maze. Results Compared with NC and Sham group, the expression of synapsinI in NT group was decreased, the escape latency was prolonged and across platform number decreased (P < 0.05). The synapses were decreased in number, and mitochondria was viewed swelling, synaptic membranes unclear, myelin fractured. Compared with NT group, the expression of synapsinⅠin HT group had no obvious change in 24 h but was significantly increased in days 3 and 14 (P < 0.01); The escape latency was decreased and the number of cross platform increased (P < 0.01); Synaptic structure was clear, with interface growing and postsynaptic density thickened. Conclusion Mild hypothermia may improve the cognitive function of the epileptic rats induced by global cerebral ischemia by upregulating the expression of synapsinⅠand alleviating the damage of synaptic structure.
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Objective To study the activity of type 2 Iodothyronine deiodinase(D2)and the expressions of myelin basic protein(MBP)and synapsinⅠin the brain tissue of young rats fed on a diet with different levels of iodine.Methods Wistar rats were fed on a diet with different doses of KIO_3 for 3 months and then mated randomly.The serum TH and the brain D2 activity were measured in 28 days old pups.The protein expressions of MBP and SynapsinⅠin their brains were determined by immunohistochemistry staining.Results Compared with normal iodine group(NI),the serum TH levels of low iodine group(LI) were lower,while those of iodine excess groups were gradually decreased with their increase of iodine intake,especially in 100-fold high iodine group(100 HI),TT_4 and FT_4 were significantly decreased(P0.05).The immunohistochemistry staining showed weakly positive reactivity of MBP in corpus callosum and stronger of synapsin I in hippocampus CA3 in LI group compared with NI. The similar alterations were also found in all iodine excess groups with their increase of iodine intake.But MBP reactivity was stronger in 100 HI rats than the LI ones.Conclusion Iodine deficiency and iodine excess can cause hypothyroidism in degrees in the young rats,more severe hypothyroid and retarded myelin sheath and synapses can be caused in iodine deficiency compared with iodine excess.
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@#ObjectiveTo study the influence of Jiuqiang Naoliqing (JNQ) on the expression of calcitonin gene related peptide(CGRP)and Synapsin Ⅰ in brain of the spontaneous hypertension rats (SHR). MethodsThe rats were randomly divided into 4 groups: Wistar group, SHR group, lower dose of JNQ treated SHR group and higher dose of JNQ treated SHR group. The expression of CGRP and Synapsin Ⅰ in the dentate gyrus, CA1 subfield of hippocampus and cortex were determined by immunohistochemistry after treatment for 3 weeks. ResultsCompared with the Wistar group, the expression of CGRP and Synapsin Ⅰ in the dentate gyrus, CA1 subfield of hippocampus and cortex of SHR group significantly decreased. The treatment with lower dose of JNQ significantly enhanced the expression of CGRP in cortex(P<0.05 vs SHR).The treatment with higher dose of JNQ significantly enhanced not only the expression of CGRP in the dentate gyrus, CA1 subfield of hippocampus and cortex, but also that of Synapsin Ⅰ in the CA1 subfield of hippocampus selectively in comparison with SHR group. ConclusionJNQ may improve the micro circulation in brain by up regulating the expression of CGRP and enhance the modulating function of central nervous system by up regulating the expression of Synapsin Ⅰ in spontaneous hypertension rats.
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Objective To illuminate relationships between epilepsy and functional and morphologic plasticity of synapse through investigating temporal-spatial expression of syanpsinⅠand the alteration of synaptic ultrastructure in hippocampus after seizure. Methods The models of epilepsy were established by injection of pilocarpine and lithium. Electromicroscope and the software of image manipulation were applied to observe the alteration of synaptic ultrastructure in hippocampus during acute phase, resting phase and chronic phase. The expressions of synapsinⅠ were determined by immunohistochemistry. Results The expression of synapsinⅠin every subfield of hippocampus decreased at 3 h after induction of seizure, reached the peak at 6 h and 12 h, which was significantly different from the control ( P
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Aim To study the effect of synapsinⅠon synaptic transmission in rat dentate gyrus induced by(-) clausenamide.Methods The basal synaptic transmission experiment was conducted through electrophysiological recordings.The effect of(-) clausenamide on synapsinⅠ phosphorylation was measured by western blot and confocal microscopy.Results(-)Clausenamide increased the population spike(PS) of hippocampal dentate gyrus.The phosphorylation of synapsinⅠ was increased both in cortex and hippocampus,the maximum effect was observed at 5 min in hippocampus and at 15 min in cortex.Furthermore,(-)clausenamide promoted the phosphorylation of synapsinⅠat a dose-denpendent manner in PC12 cells.The phosphorylation of synapsinⅠ in PC12 cells and synaptosomes incubated with(-)clausenamide was increased and reached maximum at 1~2 min.However,H89,PKA inhibitor,blocked the effect of(-)clausenamide on synapsinⅠ phosphorylation.Conclusion(-)Clausenamide activated synapsinⅠ via PKA signal pathway,which may contribute to the effect of(-)clausenamide on potentiating basal synaptic transmission.