Desjardins P, Bandeira P, Raghavendra Rao V L, Ledoux S, Butterworth R F
Neuroscience Research Unit, Hôpital Saint-Luc (University of Montreal), Que., Canada.
Brain Res. 1997 May 30;758(1-2):255-8. doi: 10.1016/s0006-8993(97)00339-9.
Using RT-PCR, gene expression of the peripheral-type benzodiazepine receptor isoquinoline carboxamide-binding protein (PTBR-IBP) was studied in the frontal cortex of rats four weeks following end-to-side portacaval anastomosis, an experimental animal model of hepatic encephalopathy, or sham operation. Portacaval anastomosis resulted in increased expression of PTBR-IBP in frontal cortex and in a concomitant increase in densities (Bmax) of binding sites for the PTBR ligand [3H]PK11195. In view of the findings that the PTBR modulates the synthesis of neurosteroids with high affinity for excitatory and inhibitory neurotransmitter systems in brain, increased expression of these receptors could be implicated in the pathogenesis of hepatic encephalopathy.
采用逆转录聚合酶链反应（RT-PCR）技术，在肝性脑病实验动物模型——端侧门腔静脉吻合术后四周的大鼠额叶皮质，或假手术组大鼠的额叶皮质中，研究外周型苯二氮䓬受体异喹啉甲酰胺结合蛋白（PTBR-IBP）的基因表达。门腔静脉吻合术导致大鼠额叶皮质中PTBR-IBP表达增加，同时PTBR配体[3H]PK11195的结合位点密度（Bmax）也随之增加。鉴于有研究发现PTBR可调节对脑中兴奋性和抑制性神经递质系统具有高亲和力的神经甾体的合成，这些受体表达增加可能与肝性脑病的发病机制有关。
