Regulation of GluA1 AMPA Receptor Through PKC Phosphorylation Induced by Free Fatty Acid Derivative HUHS2002
The present study investigated the effect of 4-[4-(Z)-hept-1-enyl-phenoxy] butyric acid (HUHS2002), a newly synthesized free fatty acid derivative, on α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor responses. HUHS2002 potentiated currents through GluA1 AMPA receptors expressed in Xenopus oocytes in a bell-shaped concentration (1 nM–1 μM)-dependent manner, the maximum reaching nearly 140 % of original amplitude at 100 nM. The potentiation was significantly inhibited by GF109203X, an inhibitor of protein kinase C (PKC), but not KN-93, an inhibitor of Ca2+/calmodulin-dependent protein kinase II (CaMKII). HUHS2002 had no potentiating effect on currents through mutant GluA1 AMPA receptors with replacement of Ser831, a PKC/CaMKII phosphorylation site, by Ala. In the in situ PKC assay using rat PC-12 cells, HUHS2002 significantly enhanced PKC activity, that is suppressed by GF109203X. Overall, the results of the present study show that HUHS2002 potentiates GluA1 AMPA receptor responses by activating PKC and phosphorylating the receptors at Ser831, regardless of CaMKII activation and phosphorylation.
- Regulation of GluA1 AMPA Receptor Through PKC Phosphorylation Induced by Free Fatty Acid Derivative HUHS2002
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Volume 48, Issue 1 , pp 23-28
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- 1. Division of Bioinformation, Department of Physiology, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, 663-8501, Japan
- 2. Laboratory of Chemical Biology, Advanced Medicinal Research Center, Hyogo University of Health Sciences, 1-3-6 Minatojima, Chuo-ku, Kobe, 650-8530, Japan