The antidepressant action of 3-(2-carboxypiperazin-4-yl) propyl-1-phosphonic acid is mediated by phosphorylation of histone deacetylase 5open access
- Authors
- Park, Min Hyeop; Choi, Miyeon; Kim, Yong-Seok; Son, Hyeon
- Issue Date
- Mar-2018
- Publisher
- KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
- Keywords
- Depression; Hippocampus; Histone deacetylase 5; NMDA receptor antagonist; Phosphorylation
- Citation
- KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY, v.22, no.2, pp.155 - 162
- Indexed
- SCIE
SCOPUS
KCI
- Journal Title
- KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
- Volume
- 22
- Number
- 2
- Start Page
- 155
- End Page
- 162
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/150428
- DOI
- 10.4196/kjpp.2018.22.2.155
- ISSN
- 1226-4512
- Abstract
- 3-(2-Carboxypiperazin-4-yl) propyl-1-phosphonic acid (CPP), a competitive N-methyl-D-aspartate (NMDA) receptor antagonist, produces rapid antidepressant-like effects in animal models of depression. However, the molecular mechanisms underlying these behavioral actions remain unknown. Here, we demonstrate that CPP rapidly stimulates histone deacetylase (HDAC) 5 phosphorylation and nuclear export in rat hippocampal neurons. These effects are accompanied by calcium/calmodulin kinase II (CaMKII) and protein kinase D (PKD) phosphorylation. Behavioral experiments revealed that viral-mediated hippocampal knockdown of HDAC5 blocked the antidepressant effects of CPP in stressed animals. Taken together, our results imply that CPP acts via HDAC5 and suggest that HDAC5 is a common regulator contributing to the antidepressant actions of NMDA receptor antagonists such as CPP.
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