Soluble Epoxide Hydrolase Inhibitor and 14,15-Epoxyeicosatrienoic Acid-Facilitated Long-Term Potentiation through cAMP and CaMKII in the Hippocampus

Epoxyeicosatrienoic acids (EETs) are derived from arachidonic acid and metabolized by soluble epoxide hydrolase (sEH). The role of EETs in synaptic function in the central nervous system is still largely unknown. We found that pharmacological inhibition of sEH to stabilize endogenous EETs and exogen...

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Veröffentlicht in:Neural plasticity. - 1998. - 2017(2017) vom: 15., Seite 3467805
1. Verfasser: Wu, Han-Fang (VerfasserIn)
Weitere Verfasser: Chen, Yi-Ju, Wu, Su-Zhen, Lee, Chi-Wei, Chen, I-Tuan, Lee, Yi-Chao, Huang, Chi-Chen, Hsing, Chung-Hsi, Tang, Chih-Wei, Lin, Hui-Ching
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2017
Zugriff auf das übergeordnete Werk:Neural plasticity
Schlagworte:Journal Article Receptors, AMPA Receptors, N-Methyl-D-Aspartate 14,15-epoxy-5,8,11-eicosatrienoic acid 81276-03-1 Cyclic AMP E0399OZS9N Calcium-Calmodulin-Dependent Protein Kinase Type 2 EC 2.7.11.17 Epoxide Hydrolases mehr... EC 3.3.2.- Ephx2 protein, mouse EC 3.3.2.10 8,11,14-Eicosatrienoic Acid FC398RK06S
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245 1 0 |a Soluble Epoxide Hydrolase Inhibitor and 14,15-Epoxyeicosatrienoic Acid-Facilitated Long-Term Potentiation through cAMP and CaMKII in the Hippocampus 
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520 |a Epoxyeicosatrienoic acids (EETs) are derived from arachidonic acid and metabolized by soluble epoxide hydrolase (sEH). The role of EETs in synaptic function in the central nervous system is still largely unknown. We found that pharmacological inhibition of sEH to stabilize endogenous EETs and exogenous 14,15-EET significantly increased the field excitatory postsynaptic potential (fEPSP) response in the CA1 area of the hippocampus, while additionally enhancing high-frequency stimulation- (HFS-) induced long-term potentiation (LTP) and forskolin- (FSK-) induced LTP. sEH inhibitor (sEHI) N-[1-(oxopropyl)-4-piperidinyl]-N'-[4-(trifluoromethoxy) phenyl)-urea (TPPU) and exogenous 14,15-EET increased HFS-LTP, which could be blocked by an N-methyl-D-aspartate (NMDA) receptor subunit NR2B antagonist. TPPU- or 14,15-EET-facilitated FSK-mediated LTP can be potentiated by an A1 adenosine receptor antagonist and a phosphodiesterase inhibitor, but is prevented by a cAMP-dependent protein kinase (PKA) inhibitor. sEHI and 14,15-EET upregulated the activation of extracellular signal-regulated kinases (ERKs) and Ca2+/calmodulin- (CaM-) dependent protein kinase II (CaMKII). Phosphorylation of synaptic receptors NR2B and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunit GluR1 was increased by TPPU and 14,15-EET administration. These results indicated that EETs increased NMDAR- and FSK-mediated synaptic potentiation via the AC-cAMP-PKA signaling cascade and upregulated the ERKs and CaMKII, resulting in increased phosphorylation of NR2B and GluR1 in the hippocampus 
650 4 |a Journal Article 
650 7 |a Receptors, AMPA  |2 NLM 
650 7 |a Receptors, N-Methyl-D-Aspartate  |2 NLM 
650 7 |a 14,15-epoxy-5,8,11-eicosatrienoic acid  |2 NLM 
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650 7 |a E0399OZS9N  |2 NLM 
650 7 |a Calcium-Calmodulin-Dependent Protein Kinase Type 2  |2 NLM 
650 7 |a EC 2.7.11.17  |2 NLM 
650 7 |a Epoxide Hydrolases  |2 NLM 
650 7 |a EC 3.3.2.-  |2 NLM 
650 7 |a Ephx2 protein, mouse  |2 NLM 
650 7 |a EC 3.3.2.10  |2 NLM 
650 7 |a 8,11,14-Eicosatrienoic Acid  |2 NLM 
650 7 |a FC398RK06S  |2 NLM 
700 1 |a Chen, Yi-Ju  |e verfasserin  |4 aut 
700 1 |a Wu, Su-Zhen  |e verfasserin  |4 aut 
700 1 |a Lee, Chi-Wei  |e verfasserin  |4 aut 
700 1 |a Chen, I-Tuan  |e verfasserin  |4 aut 
700 1 |a Lee, Yi-Chao  |e verfasserin  |4 aut 
700 1 |a Huang, Chi-Chen  |e verfasserin  |4 aut 
700 1 |a Hsing, Chung-Hsi  |e verfasserin  |4 aut 
700 1 |a Tang, Chih-Wei  |e verfasserin  |4 aut 
700 1 |a Lin, Hui-Ching  |e verfasserin  |4 aut 
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