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.
出处
《上海医科大学学报》
CSCD
1995年第4期266-268,共3页
Journal of Fudan University(Medical Science)
关键词
胆囊收缩素
脑啡肽
脑损伤
原位杂交
MRNA
preprocholecystokinin
preproenkephalin:in situ hybridization
brain injury
