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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| Format: | Article |
| Language: | English |
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Wiley
2017-01-01
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| Series: | Neural Plasticity |
| Online Access: | http://dx.doi.org/10.1155/2017/3467805 |
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| author | Han-Fang Wu Yi-Ju Chen Su-Zhen Wu Chi-Wei Lee I-Tuan Chen Yi-Chao Lee Chi-Chen Huang Chung-Hsi Hsing Chih-Wei Tang Hui-Ching Lin |
| author_facet | Han-Fang Wu Yi-Ju Chen Su-Zhen Wu Chi-Wei Lee I-Tuan Chen Yi-Chao Lee Chi-Chen Huang Chung-Hsi Hsing Chih-Wei Tang Hui-Ching Lin |
| author_sort | Han-Fang Wu |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-ef3d991706ae413fa6ff50506c182736 |
| institution | Kabale University |
| issn | 2090-5904 1687-5443 |
| language | English |
| publishDate | 2017-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Neural Plasticity |
| spelling | doaj-art-ef3d991706ae413fa6ff50506c1827362025-02-03T06:06:09ZengWileyNeural Plasticity2090-59041687-54432017-01-01201710.1155/2017/34678053467805Soluble Epoxide Hydrolase Inhibitor and 14,15-Epoxyeicosatrienoic Acid-Facilitated Long-Term Potentiation through cAMP and CaMKII in the HippocampusHan-Fang Wu0Yi-Ju Chen1Su-Zhen Wu2Chi-Wei Lee3I-Tuan Chen4Yi-Chao Lee5Chi-Chen Huang6Chung-Hsi Hsing7Chih-Wei Tang8Hui-Ching Lin9Department and Institute of Physiology, School of Medicine, National Yang-Ming University, Taipei, TaiwanDepartment and Institute of Physiology, School of Medicine, National Yang-Ming University, Taipei, TaiwanDepartment of Anesthesiology, Chi-Mei Medical Center, Tainan, TaiwanDepartment and Institute of Physiology, School of Medicine, National Yang-Ming University, Taipei, TaiwanDepartment and Institute of Physiology, School of Medicine, National Yang-Ming University, Taipei, TaiwanGraduate Institute of Neural Regenerative Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei, TaiwanGraduate Institute of Neural Regenerative Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei, TaiwanDepartment of Anesthesiology, Chi-Mei Medical Center, Tainan, TaiwanDepartment of Neurology, Far Eastern Memorial Hospital, New Taipei City, TaiwanDepartment and Institute of Physiology, School of Medicine, National Yang-Ming University, Taipei, TaiwanEpoxyeicosatrienoic 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.http://dx.doi.org/10.1155/2017/3467805 |
| spellingShingle | Han-Fang Wu Yi-Ju Chen Su-Zhen Wu Chi-Wei Lee I-Tuan Chen Yi-Chao Lee Chi-Chen Huang Chung-Hsi Hsing Chih-Wei Tang Hui-Ching Lin Soluble Epoxide Hydrolase Inhibitor and 14,15-Epoxyeicosatrienoic Acid-Facilitated Long-Term Potentiation through cAMP and CaMKII in the Hippocampus Neural Plasticity |
| title | Soluble Epoxide Hydrolase Inhibitor and 14,15-Epoxyeicosatrienoic Acid-Facilitated Long-Term Potentiation through cAMP and CaMKII in the Hippocampus |
| title_full | Soluble Epoxide Hydrolase Inhibitor and 14,15-Epoxyeicosatrienoic Acid-Facilitated Long-Term Potentiation through cAMP and CaMKII in the Hippocampus |
| title_fullStr | Soluble Epoxide Hydrolase Inhibitor and 14,15-Epoxyeicosatrienoic Acid-Facilitated Long-Term Potentiation through cAMP and CaMKII in the Hippocampus |
| title_full_unstemmed | Soluble Epoxide Hydrolase Inhibitor and 14,15-Epoxyeicosatrienoic Acid-Facilitated Long-Term Potentiation through cAMP and CaMKII in the Hippocampus |
| title_short | Soluble Epoxide Hydrolase Inhibitor and 14,15-Epoxyeicosatrienoic Acid-Facilitated Long-Term Potentiation through cAMP and CaMKII in the Hippocampus |
| title_sort | soluble epoxide hydrolase inhibitor and 14 15 epoxyeicosatrienoic acid facilitated long term potentiation through camp and camkii in the hippocampus |
| url | http://dx.doi.org/10.1155/2017/3467805 |
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