OBJECTIVES: Estrogen regulates a wide variety of nonreproductive functions in the central nervous system. Cortical neurons contain a diverse range of voltage-gated ion channels, including calcium (Ca(2+)) channels, and Ca(2+) channels play an important role in the regulation of action potential generation and neuronal excitability. In this study, the effect of estradiol (E2) on high-voltage-activated (HVA) Ca(2+) channels in cultured rat cortical neurons was examined. METHODS: We used the whole-cell patch-clamp technique to measure the HVA Ca(2+) channels. RESULTS: We found that HVA Ca(2+) channel currents was inhibited by 17β-E2 in a rapid, reversible and concentration-dependent manner. Moreover, 17β-E2 shifted the steady-state inactivation curve in the hyperpolarizing direction without changing the activation curve. We also found that the inhibitory effects of 17β-E2 on Ca(2+) currents were unaffected by the estrogen receptor (ER) antagonist ICI 182780; however, the protein kinase C (PKC) inhibitor rottlerin and protein kinase A (PKA) inhibitor H-89 blocked the 17β-E2-induced inhibition of Ca(2+) currents. CONCLUSIONS: E2 inhibited HVA Ca(2+) currents via PKC and PKA-dependent signaling pathway in cortical neurons, and the effects of BPA were independent of classical ER.
OBJECTIVES: Estrogen regulates a wide variety of nonreproductive functions in the central nervous system. Cortical neurons contain a diverse range of voltage-gated ion channels, including calcium (Ca(2+)) channels, and Ca(2+) channels play an important role in the regulation of action potential generation and neuronal excitability. In this study, the effect of estradiol (E2) on high-voltage-activated (HVA) Ca(2+) channels in cultured rat cortical neurons was examined. METHODS: We used the whole-cell patch-clamp technique to measure the HVA Ca(2+) channels. RESULTS: We found that HVA Ca(2+) channel currents was inhibited by 17β-E2 in a rapid, reversible and concentration-dependent manner. Moreover, 17β-E2 shifted the steady-state inactivation curve in the hyperpolarizing direction without changing the activation curve. We also found that the inhibitory effects of 17β-E2 on Ca(2+) currents were unaffected by the estrogen receptor (ER) antagonist ICI 182780; however, the protein kinase C (PKC) inhibitor rottlerin and protein kinase A (PKA) inhibitor H-89 blocked the 17β-E2-induced inhibition of Ca(2+) currents. CONCLUSIONS: E2 inhibited HVA Ca(2+) currents via PKC and PKA-dependent signaling pathway in cortical neurons, and the effects of BPA were independent of classical ER.
Authors: Juan Du; Qiang Wang; Fang Hu; Jun Wang; Haixia Ding; Rong Gao; Hang Xiao; Lin Wang Journal: J Membr Biol Date: 2014-05-17 Impact factor: 1.843
Authors: Adela Banciu; Daniel Dumitru Banciu; Cosmin Catalin Mustaciosu; Mihai Radu; Dragos Cretoiu; Junjie Xiao; Sanda Maria Cretoiu; Nicolae Suciu; Beatrice Mihaela Radu Journal: Int J Mol Sci Date: 2018-05-09 Impact factor: 5.923