Kinoshita Ken-Ichi, Muroi Yoshikage, Unno Toshihiro, Ishii Toshiaki
Department of Pathogenetic Veterinary Science, United Graduate School of Veterinary Sciences, Gifu University, 1-1 Yanagido, Gifu 501-1193, Japan.
Department of Pathogenetic Veterinary Science, United Graduate School of Veterinary Sciences, Gifu University, 1-1 Yanagido, Gifu 501-1193, Japan; Department of Basic Veterinary Medicine, Obihiro University of Agriculture and Veterinary Medicine, Obihiro, Hokkaido 080-8555, Japan.
J Pharmacol Sci. 2017 May;134(1):55-58. doi: 10.1016/j.jphs.2017.04.002. Epub 2017 Apr 17.
Cognitive impairment often occurs in Parkinson's disease (PD), but the mechanism of onset remains unknown. Recently, we reported that PD model mice produced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) show facilitation of hippocampal memory extinction, which may be the cause of cognitive impairment in PD. When we examined the cAMP/CREB signaling in the hippocampus, decreased levels of cAMP and phosphorylated CREB were observed in the dentate gyrus (DG) of MPTP-treated mice. Administration of rolipram improved the memory deficits with concomitant recovery of cAMP and phosphorylated CREB levels, suggesting that reduced cAMP/CREB signaling in the DG leads to cognitive impairment in MPTP-treated mice.
认知障碍常发生于帕金森病（PD），但其发病机制尚不清楚。最近，我们报道1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）制备的PD模型小鼠表现出海马记忆消退的易化，这可能是PD认知障碍的原因。当我们检测海马中的cAMP/CREB信号通路时，在MPTP处理的小鼠齿状回（DG）中观察到cAMP和磷酸化CREB水平降低。给予咯利普兰改善了记忆缺陷，同时cAMP和磷酸化CREB水平恢复，表明DG中cAMP/CREB信号通路的减少导致MPTP处理小鼠的认知障碍。
