ArticleCellular and molecular neurobiology2010
Estradiol inhibits depolarization-evoked exocytosis in PC12 cells via N-type voltage-gated calcium channels.
Article in Cellular and molecular neurobiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 10 citations in OpenAlex.
- The effects of 17 alpha-estradiol to inhibit inflammation in vitro.Biology of sex differences · 2017Article
- The effects of different doses of estradiol (E2) on cerebral ischemia in an in vitro model of oxygen and glucose deprivation and reperfusion and in a rat model of middle carotid artery occlusion.BMC neuroscience · 2013Article
- Chemical analysis of single cells.Analytical chemistry · 2011Review
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Authors and funding
5 authors at 3 institutions in 3 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Fast neuromodulatory effects of 17-β-estradiol (E2) on cytosolic calcium concentration ([Ca(2+)](i)) have been reported in many cell types, but little is known about its direct effects on vesicular neurotransmitter secretion (exocytosis). We examined the effects of E2 on depolarization-evoked [Ca(2+)](i) in PC12 cells using fluorescence measurements. Imaging of [Ca(2+)](i) with FURA-2 revealed that depolarization-evoked calcium entry is inhibited after exposure to 10 nM and 10 μM E2. Calcium entry after exposure to 50 μM E2 decreases slightly, but insignificantly. To relate E2-induced changes in [Ca(2+)](i) to functional effects, we measured exocytosis using amperometry. It was observed that E2 in some cells elicits exocytosis upon exposure. In addition, E2 inhibits depolarization-evoked exocytosis with a complex concentration dependence, with inhibition at both physiological and pharmacological concentrations. This rapid inhibition amounts to 45% at a near physiological level (10 nM E2), and 50% at a possible pharmacological concentration of 50 μM. A small percentage (22%) of cells show exocytosis during E2 exposure ("Estrogen stimulated"), thus vesicle depletion could possibly account (at least partly) for the E2-induced inhibition of depolarization-evoked exocytosis. In cells that do not exhibit E2-stimulated release ("Estrogen quiet"), the E2-induced inhibition of exocytosis is abolished by a treatment that eliminates the contribution of N-type voltage-gated calcium channels (VGCCs) to exocytosis. Overall, the data suggest that E2 can act on N-type VGCCs to affect secretion of neurotransmitters. This provides an additional mechanism for the modulation of neuronal communication and plasticity by steroids.
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