Abstract
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 (Ca2+) channels, and Ca2+ 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) Ca2+ channels in cultured rat cortical neurons was examined. Methods: We used the whole-cell patch-clamp technique to measure the HVA Ca2+ channels. Results: We found that HVA Ca2+ 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 Ca2+ 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 Ca2+ currents. Conclusions: E2 inhibited HVA Ca2+ currents via PKC and PKA-dependent signaling pathway in cortical neurons, and the effects of BPA were independent of classical ER.
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