@article {Dayanithi130, author = {G Dayanithi and L Tapia-Arancibia}, title = {Rise in intracellular calcium via a nongenomic effect of allopregnanolone in fetal rat hypothalamic neurons}, volume = {16}, number = {1}, pages = {130--136}, year = {1996}, doi = {10.1523/JNEUROSCI.16-01-00130.1996}, publisher = {Society for Neuroscience}, abstract = {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{\textendash}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.}, issn = {0270-6474}, URL = {https://www.jneurosci.org/content/16/1/130}, eprint = {https://www.jneurosci.org/content/16/1/130.full.pdf}, journal = {Journal of Neuroscience} }