Anti-epileptic effects of neuropeptide Y gene transfection into the rat brain

来源 :Neural Regeneration Research | 被引量 : 0次 | 上传用户:eyx001
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Neuropeptide Y gene transfection into normal rat brain tissue can provide gene overexpression,which can attenuate the severity of kainic acid-induced seizures.In this study,a recombinant adeno-associated virus carrying the neuropeptide Y gene was transfected into brain tissue of rats with kainic acid-induced epilepsy through stereotactic methods.Following these transfections,we verified overexpression of the neuropeptide Y gene in the epileptic brain.Electroencephalograms showed that seizure severity was significantly inhibited and seizure latency was significantly prolonged up to 4 weeks after gene transfection.Moreover,quantitative fluorescent PCR and western blot assays revealed that the mRNA and protein expression of the N-methyl-D-aspartate receptor subunits NR1,NR2A,and NR2B was inhibited in the hippocampus of epileptic rats.These findings indicate that neuropeptide Y may inhibit seizures via down-regulation of the functional expression of N-methyl-D-aspartate receptors. Neuropeptide Y gene transfection into normal rat brain tissue can provide gene overexpression, which can attenuate the severity of kainic acid-induced seizures. In this study, a recombinant adeno-associated virus carrying the neuropeptide Y gene was transfected into brain tissue of rats with kainic acid-induced epilepsy through stereotactic methods. Folly these transfections, we verified overexpression of the neuropeptide Y gene in the epileptic brain. Electroencephalogram showed that seizure severity was significantly inhibited and seizure latency was significantly prolonged up to 4 weeks after gene transfection. Moreover, quantitative fluorescent PCR and western blot assays revealed that the mRNA and protein expression of the N-methyl-D-aspartate receptor subunits NR1, NR2A, and NR2B was inhibited in the hippocampus of epileptic rats. These findings that that neuropeptide Y may inhibit seizures via -regulation of the functional expression of N-methyl-D-aspartate receptors.
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