Journal
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
Volume 21, Issue 1-3, Pages 161-172Publisher
KARGER
DOI: 10.1159/000113758
Keywords
gonadal steroid hormone; central nervous system; neuron; retina; electrophysiology; kinase
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Funding
- NATIONAL CENTER ON MINORITY HEALTH AND HEALTH DISPARITIES [P20MD001633] Funding Source: NIH RePORTER
- NATIONAL EYE INSTITUTE [R01EY014227] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [T32AG020494, P01AG027956, P01AG022550, P01AG010485] Funding Source: NIH RePORTER
- NEI NIH HHS [EY014227, R01 EY014227] Funding Source: Medline
- NIA NIH HHS [AG022550, P01 AG010485, AG010485, AG027956, T32 AG020494, P01 AG027956, P01 AG022550] Funding Source: Medline
- NIMHD NIH HHS [MD001633] Funding Source: Medline
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The activity of cells critically depends on the control of their cytosolic free calcium ion (Ca2+) concentration. The objective of the present study was to identify mechanisms of action underlying the control of the gain of intracellular Ca2+ release by circulating gonadal steroid hormones. Acute stimulation of isolated neurons with progesterone led to IP3 R-mediated Ca2+ 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 IP3 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 Ca2+ 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. Copyright (c) 2008 S. Karger AG, Basel.
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