Key result
Progesterone rapidly shifts mouse skeletal muscle ClC-1 activation curves more strongly than 17β-estradiol.
Why the study?
Do progesterone and 17β-estradiol modulate chloride conductance in mouse skeletal muscle?
Do progesterone and 17β-estradiol modulate chloride conductance in mouse skeletal muscle?
High concentrations of sex hormones can rapidly modulate ClC-1 chloride channels in mammalian skeletal muscle through a nongenomic mechanism, which may relate to the exacerbation of myotonia congenita during pregnancy.
INTRODUCTION: Myotonia congenita, caused by mutations in ClC-1, tends to be more severe in men and is often exacerbated by pregnancy. METHODS: We performed whole-cell patch clamp of mouse muscle chloride currents in the absence/presence of 100 μM progesterone or 17β-estradiol. RESULTS: 100 μM progesterone rapidly and reversibly shifted the ClC-1 activation curve of mouse skeletal muscle (V50 changed from -52.6 ± 9.3 to +35.5 ± 6.7; P < 0.01) and markedly reduced chloride currents at depolarized potentials. 17β-estradiol at the same concentration had a similar but smaller effect (V50 change from -57.2 ± 7.6 to -40.5 ± 9.8; P < 0.05). 1 μM progesterone produced no significant effect. CONCLUSIONS: Although the data support the existence of a nongenomic mechanism in mammalian skeletal muscle through which sex hormones at high concentration can rapidly modulate ClC-1, the influence of hormones on muscle excitability in vivo remains an open question.
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Burge et al. (2013) studied Myotonia congenita. Progesterone and 17β-estradiol vs. Absence of hormones was evaluated on ClC-1 activation curve (V50) (p=<0.01). 100 μM progesterone rapidly shifted the ClC-1 activation curve of mouse skeletal muscle (V50 changed from -52.6 to +35.5; P<0.01), while 17β-estradiol had a similar but smaller effect (P<0.05).
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