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Objective To analyze the expression of cholecystokinin(CCK) in rat' s hippocampus and cerebral cortex following heat stress and febrile convulsions (FC). Methods Warm water was used to induce FC model. Immunohistochemistry method tested CCK protein. Results Very few or no CCK neurons were seen in the control rats. There was weaker expression of CCK in cerebral cortex of HS group,mainly located in PIR,ENT and RS subfield.No CCK positive ceiis were seen in hippocampus of HS rats. In contrast, abundant expression of CCK protein was found in hippocampus and cerebral cortex of FC group. They were well-distributed, without characteristic subnucleus-specific distribution. Conclusion Abundant induction of CCK in hippocampus and cerebral cortex of FC group suggested that CCK may play a role in the central control of FC.
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Objective To analyze the expression of prolactin protein and ZnT1 mRNA in rat brain in the wake of heat stress and febrile convulsion(FC).Method Thirty-six weanling Spragne-Dawley rats were randomly divided into control group(n=8) and other 28 rats were used to induce heat stroke by warm water but three of them failed to produc expected heat stress.Consequently,there were 35 rats eligible to be models of heat stroke,and of them,10 rats showed heat stress(HS group,n=10) and 15 rats had 5-grade febrile convulsion (FC group,n = 15).The inmmunohistocbemistry and in situ hybridization method were used in this study.The IR) neurons were found in the rats of control group.The deep immune staining was found in the PIR,Era and RS regions of cerebral cortex and light immune staining was found in the PRH,PAR and FR regions of cerebral cortex in HS group.In addition,the PRL-IR positive neurons were found around the midline strip of thalamus without characteristic subnucleus-specific distribution.However,abundant induction of PRL-IR positive neurons with diffuse distribution were found in cerebral cortex,hippoeampus,amygdala,thalamus and hypotha]amns of rats in FC and FC rats showed more PRD-IR positive neurons in cerebral cortex than those in rats of control group (P<ZnT3 mRNA positive cells were seen in I-IS and control group.In contrast,abundant induction of ZnT3 mRNA There is an elevated zinc metabolism in hippocampus of FC group.
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Objective To investigate the relationship between dexamethasone and brain derive neurotrophic factor gene in experimental bacterial meningitis. Methods To construct the models of bacterial meningitis in 3 weeks old rats(n=33),then 23 of them were administed antibiotic and antibiotic plus dexamethasone respectively. BDNF mRNA and TrkB mRNA in brain was detected by in situ hybridization methods,respectively. Results After administration antibiotics, the expression of BDNF mRNA and TrkB mRNA in brain tissue were less than that in brain after infection 5 d(P 0.05), the expression of TrkB mRNA was stronger than that in brain at 5 d after infection(P
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AIM: To investigate the expression and effect of brain derived neurotrophic factor (BDNF) mRNA and its protein in infancy rats after exposure to bacterial meningitis. METHODS: Three week old rats were used to construct the models of bacterial meningitis (n=30) and mormal(n=18). At 24 h, 48 h, 5 d after inoculating, the expression of BDNF mRNA and its protein were detected by in situ hybridization and immunohistochemical staining methods, respectively. RESULTS: The increase in BDNF mRNA expression was detected by in situ hybridization at 24 h in experiment( 0.13320? 0.02750) compared to control( 0.06269? 0.01147)(P0.05). Meanwhile, in the brain from the experiment rats, strong positive hybridization and immunoreactivity were observed in the infiltrated inflammatory cells in leptomeninges, subarachnoid cavity, ventricles and brain parenchyma. CONCLUSIONS: These results support the hypothesis that BDNF might play a neuroprotective role in brain damage process in bacterial meningitis attacked rats. BDNF might take part in imune response. These results also support the hypothesis that BDNF has some relationships with other inflammatory mediators during acute inflammatory response of bacterial meningitis.
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AIM: To investigate the effects of diazoxide, an ATP-sensitive K + channel opener on the ?-calpain activation, c-Fos and c- Jun expression in neonatal hypoxic-ischemic rat brain. METHODS:The animal model of hypoxic-ischemic brain injury (HIBI) was made in the 7-day -old SD rats. Diazoxide was injected into the left lateral ventricle prior or po st hypoxic-ischemia (HI) insults. Western blot was applied to detect the integra ted density (ID) of the nuclear c-Fos and c-Jun at 4h, and the cleavage of cytos olic ?-calpain at 24 h after HI insults. RESULTS: Low c-Fos and c-Jun expressions from cortical and hippocampal samples were observed in the tw o diazoxide groups, and significant differences in their expressions were found by comparison with the HI controls (P