Journal
NEUROSCIENCE LETTERS
Volume 586, Issue -, Pages 24-30Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2014.12.010
Keywords
Dopamine; GABA; ERK; Hippocampal neurons; Dendritic spine
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Funding
- Mid-Career Researcher Program from National Research Foundation of Korea (NRF) grant - Korea Government (MSIP) [2014R1A2A2A01003337]
- Korea University Grant
- National Research Foundation of Korea [2014R1A2A2A01003337] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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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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