| Literature DB >> 28456375 |
Ken-Ichi Kinoshita1, Yoshikage Muroi2, Toshihiro Unno3, Toshiaki Ishii4.
Abstract
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.Entities:
Keywords: MPTP-Treated mice; Memory extinction; Phosphodiesterase IV inhibitor rolipram
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Year: 2017 PMID: 28456375 DOI: 10.1016/j.jphs.2017.04.002
Source DB: PubMed Journal: J Pharmacol Sci ISSN: 1347-8613 Impact factor: 3.337