Rise in intracellular calcium via a nongenomic effect of allopregnanolone in fetal rat hypothalamic neurons.
نویسندگان
چکیده
This study examines the early effects of 3 alpha-hydroxy-5 alpha-pregnan-20-one (allopregnanolone on cytosolic free calcium concentration ([Ca2+]i in primary cultures of fetal rat hypothalamic neurons. Microspectrofluorimetry of fluorescent Ca2+(-)sensitive indicator Fura-2 was used to quantify these changes. Allopregnanolone (1 pM to 100 nM) increased [Ca2+]i within 2-3 sec, in a dose dependent manner, with an EC50 of 10 +/- 4 nM. The stimulatory effect of allopregnanolone was attributable principally to a Ca2+ influx, as shown by the strong inhibition of external Ca2+ removal or by the calcium channel blocker nifedipine. The effect was stereospecific because the allopregnanolone isomer 3 beta-hydroxy-5 alpha-pregnan-20-one had no effect on [Ca2+]i. Among two other steroids examined, progesterone had no effect on [Ca2+]i, but 17 beta-estradiol evoked a rise in [Ca2+]i, although to a lesser extent than allopregnanolone. The allopregnanolone-induced [Ca2+]i rise was inhibited by picrotoxin and bicuculline but was unaffected by tetrodotoxin or by pretreatment of neurons with pertussis toxin. These results are consistent with a membrane site of action for allopregnanolone associated with GABAA receptors, leading to rapid changes in [Ca2+]i in fetal rat hypothalamic neurons.
منابع مشابه
The neurosteroid allopregnanolone promotes proliferation of rodent and human neural progenitor cells and regulates cell-cycle gene and protein expression.
Our previous research demonstrated that the neuroactive progesterone metabolite allopregnanolone (3alpha-hydroxy-5alpha-pregnan-20-one) rapidly induced hippocampal neuron neurite regression (Brinton, 1994). We hypothesized that allopregnanolone-induced neurite regression was a prelude to mitogenesis initiated by a rise in intracellular calcium. Supporting this hypothesis, the current data demon...
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ورودعنوان ژورنال:
- The Journal of neuroscience : the official journal of the Society for Neuroscience
دوره 16 1 شماره
صفحات -
تاریخ انتشار 1996