Journal
BRAIN RESEARCH
Volume 1512, Issue -, Pages 1-8Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.brainres.2013.02.047
Keywords
Estradiol; Voltage-gated sodium channels; Dorsal root ganglion neurons
Categories
Funding
- Fund of Jiangsu University for Advanced Scholars [12JDG083]
- National Natural Science Foundation of China [81072329]
- Priority Academic Program Development (PAPD) of Jiangsu Higher Education Institutions
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Estrogen has multiple actions in the brain to modulate homeostasis, synaptic plasticity, neuroprotection and pain sensitivity Previous studies have demonstrated that estradiol may affect the ion channel function. The role of voltage-gated sodium channels in the transmission of nociceptive and neuropathic pain messages is well-established. Herein, we report the effects of estradiol (E2) on TTX-sensitive (TTX-S) and TTX-resistant (TTX-R) Na+ currents, using a conventional whole-cell patch clamp technique from acutely isolated mouse dorsal root ganglion neurons. We found that the extracellularly 17 beta-E2 inhibited TTX-S Na+ currents and TTX-R Na+ currents; the effects were rapid, reversible and in a concentration-dependent manner. Moreover, 17 beta-E2 did not significantly affect the activation curve for Na+ channel, and shifted the steady-state inactivation curve for TTX-S and TTX-R Na+ channels in the hyperpolarizing direction. We also found that the membrane impermeable E2-BSA was as efficacious as 17 beta-E2, whereas 17 alpha-E2 had no effect. Blockers of PKC (GO-6983) and PKA (H-89) abrogated these acute effects of 17 beta-E2. In conclusion, E2 inhibited voltage-gated Na+ channels in mouse DRG neurons through a membrane ER-activated PKC-PKA signaling pathway. Through the modulation of voltage-gated sodium currents, estradiol could affect cell excitability, firing properties. (C) 2013 Elsevier BV All rights reserved.
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