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Updated: Jul 8, 2026

Direct Imaging of ER Calcium with Targeted-Esterase Induced Dye Loading (TED)
Published on: May 7, 2013
Progesterone potentiates IP(3)-mediated calcium signaling through Akt/PKB
Peter Koulen1, Christian Madry, R Scott Duncan
1Department of Pharmacology and Neuroscience, University of North Texas Health Science Center at Fort Worth, Fort Worth, TX 76107-2699, USA. pkoulen@hsc.unt.edu
Abstract:
The activity of cells critically depends on the control of their cytosolic free calcium ion (Ca(2+)) concentration. The objective of the present study was to identify mechanisms of action underlying the control of the gain of intracellular Ca(2+) release by circulating gonadal steroid hormones. Acute stimulation of isolated neurons with progesterone led to IP(3)R-mediated Ca(2+) transients that depend on the activation of the PI3 kinase/Akt/PKB signaling pathway. These results were confirmed at the molecular level and phosphorylation of IP(3)R type 1 by Akt/PKB was identified as the mechanism of action. Hence, it is likely that circulating gonadal steroid hormones control neuronal activity including phosporylation status through receptor- and kinase-mediated signaling. With a direct control of the gain of the Ca(2+) second messenger system as a signaling gatekeeper for neuronal activity the present study identifies a novel pathway for interaction of the endocrine and central nervous system.
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