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- Takafumi Horishita, Susumu Ueno, Nobuyuki Yanagihara, Yuka Sudo, Yasuhito Uezono, Dan Okura, and Takeyoshi Sata.
- Department of Anesthesiology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan. thori@med.uoeh-u.ac.jp
- J. Pharmacol. Sci. 2012 Jan 1;120(1):54-8.
AbstractNeurosteroids are known as allosteric modulators of the ligand-gated ion channel superfamily. Voltage-gated sodium channels (Na(v)) play an important role in mediating excitotoxic damages. Here we report the effects of neurosteroids on the function of Na(v), using voltage-clamp techniques in Xenopus oocytes expressed with the Na(v)1.2 α subunit. Pregnenolone sulphate, but not pregnenolone, inhibited sodium currents (I(Na)) at 3 - 100 μmol/L. The suppression of I(Na) by pregnenolone sulphate was due to increased inactivation with little change in activation. These findings suggest that pregnenolone sulphate, a metabolite of pregnenolone, suppresses the function of Na(v) via increased inactivation, which may contribute to the neuroprotection.
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