Progesterone potentiates IP                         3                         -mediated calcium signaling through Akt/PKB

Peter Koulen; Christian Madry; R. Scott Duncan; Ji Yeon Hwang; Everett Nixon; Nathalie McClung; Elaine V. Gregg; Meharvan Singh

doi:10.1159/000113758

Progesterone potentiates IP ₃ -mediated calcium signaling through Akt/PKB

Peter Koulen, Christian Madry, R. Scott Duncan, Ji Yeon Hwang, Everett Nixon, Nathalie McClung, Elaine V. Gregg, Meharvan Singh

Pharmacology & Neuroscience

Research output: Contribution to journal › Article › peer-review

33 Scopus citations

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.

Original language	English
Pages (from-to)	161-172
Number of pages	12
Journal	Cellular Physiology and Biochemistry
Volume	21
Issue number	1-3
DOIs	https://doi.org/10.1159/000113758
State	Published - 2008

Keywords

Central nervous system
Electrophysiology
Gonadal steroid hormone
Kinase
Neuron
Retina

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10.1159/000113758

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title = " Progesterone potentiates IP 3 -mediated calcium signaling through Akt/PKB ",

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.",

keywords = "Central nervous system, Electrophysiology, Gonadal steroid hormone, Kinase, Neuron, Retina",

author = "Peter Koulen and Christian Madry and Duncan, {R. Scott} and Hwang, {Ji Yeon} and Everett Nixon and Nathalie McClung and Gregg, {Elaine V.} and Meharvan Singh",

year = "2008",

doi = "10.1159/000113758",

language = "English",

volume = "21",

pages = "161--172",

journal = "Cellular Physiology and Biochemistry",

issn = "1015-8987",

publisher = "S. Karger AG",

number = "1-3",

}

Progesterone potentiates IP ₃ -mediated calcium signaling through Akt/PKB . / Koulen, Peter; Madry, Christian; Duncan, R. Scott et al.
In: Cellular Physiology and Biochemistry, Vol. 21, No. 1-3, 2008, p. 161-172.

Research output: Contribution to journal › Article › peer-review

TY - JOUR

T1 - Progesterone potentiates IP 3 -mediated calcium signaling through Akt/PKB

AU - Koulen, Peter

AU - Madry, Christian

AU - Duncan, R. Scott

AU - Hwang, Ji Yeon

AU - Nixon, Everett

AU - McClung, Nathalie

AU - Gregg, Elaine V.

AU - Singh, Meharvan

PY - 2008

Y1 - 2008

N2 - 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.

AB - 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.

KW - Central nervous system

KW - Electrophysiology

KW - Gonadal steroid hormone

KW - Kinase

KW - Neuron

KW - Retina

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U2 - 10.1159/000113758

DO - 10.1159/000113758

M3 - Article

C2 - 18209483

AN - SCOPUS:38549095165

SN - 1015-8987

VL - 21

SP - 161

EP - 172

JO - Cellular Physiology and Biochemistry

JF - Cellular Physiology and Biochemistry

IS - 1-3

ER -

Progesterone potentiates IP ₃ -mediated calcium signaling through Akt/PKB

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Keywords

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