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出 处:《上海医科大学学报》1995年第4期266-268,共3页Journal of Fudan University(Medical Science)
摘 要:应用原位杂交技术,研究大鼠脑损伤后前胆囊收缩素(PCCK)和前脑啡肽原(PPE)mRNA的表达。结果表明,在大鼠脑损伤24h后同侧脑内PCCK和PPEmRNA量增加,尤其以新皮质和海马显著。给予NMDA受体非竞争性拮抗剂ketamine可以抑制增加。因此,作者认为在脑损伤后可诱发胆囊收缩素(CCK)和脑啡肽(ENK)合成增加,并参与脑损伤病理改变,另外这种合成增加可能由NMDA受体介导。Using in situ hybridization method, alteration of the mRNA concentration of both the preprocholecystokin(PCCK) and preproenkephalin(PPE) after rat brain injury and the mechenism of this trauma inducing change in neuropeptide neuropeptide gene expression were analysed. The results showed that 48h after in jury of the rat brain,the concentration of mRNA coding for PPE,and PCCK was increased significantly in ipsilateral side specially in the cortical area,hippocampus.The ketamine, a N-methyl-D-aspartate receptor non-competetive antagonist,can prevented the injury-induced increase in both PCCK and PPE gene expression. So,it is hypothetized that the brai injury can activate the PPE, PCCK neuropeptide gene which may be mediated by NMDA receptor.
分 类 号:R651.150.2[医药卫生—外科学]
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