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Regulation of dopamine D2 receptor-mediated extracellular signal-regulated kinase signaling and spine formation by GABA(A) receptors in hippocampal neurons

Authors
Yoona, Dong-HoonYoon, SehyounKim, DonghoonKim, HyunBaik, Ja-Hyun
Issue Date
23-1월-2015
Publisher
ELSEVIER IRELAND LTD
Keywords
Dopamine; GABA; ERK; Hippocampal neurons; Dendritic spine
Citation
NEUROSCIENCE LETTERS, v.586, pp.24 - 30
Indexed
SCIE
SCOPUS
Journal Title
NEUROSCIENCE LETTERS
Volume
586
Start Page
24
End Page
30
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/94621
DOI
10.1016/j.neulet.2014.12.010
ISSN
0304-3940
Abstract
Dopamine (DA) signaling via DA receptors is known to control hippocampal activity that contributes to learning, memory, and synaptic plasticity. In primary hippocampal neuronal culture, we observed that dopamine D2 receptors (D2R) co-localized with certain subtypes of GABA(A) receptors, namely oil, (33, and gamma 2 subunits, as revealed by double immunofluorocytochemical analysis. Treatment with the D2R agonist, quinpirole, was shown to elicit an increase in phosphorylation of extracellular signal-regulated kinase (ERK) in hippocampal neurons. This phosphorylation was inhibited by pretreatment with the GABA(A) receptor agonist, muscimol. Furthermore, treatment of hippocampal neurons with quinpirole increased the dendritic spine density and this regulation was totally blocked by pretreatment with a MAP kinase kinase (MEK) inhibitor (PD98059), D2R antagonist (haloperidol), or by the GABA(A) receptor agonist, muscimol. These results suggest that D2R-mediated ERK phosphorylation can control spine formation and that the GABA(A) receptor negatively regulates the D2R-induced spine formation through ERK signaling in hippocampal neurons, thus indicating a potential role of D2R in the control of hippocampal neuronal excitability. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
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