Insulin inhibits voltage-dependent calcium influx into rod photoreceptors

Jr Stella; E. J. Bryson; W. B. Thoreson

doi:10.1097/00001756-200104170-00017

Insulin inhibits voltage-dependent calcium influx into rod photoreceptors

Jr Stella, E. J. Bryson, W. B. Thoreson

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

24 Scopus citations

Abstract

Insulin inhibits the ERG b-wave and modulates L-type calcium currents (I_Ca) in various preparations. We therefore examined insulin's effects on I_Ca and depolarization-evoked [Ca²⁺]_i increases in rod photoreceptors. Insulin inhibited I_Ca and caused a dose-dependent reduction in the depolarization-evoked Ca²⁺ influx with an EC₅₀ of 2.1 nM. Tyrosine kinase inhibitors, lavendustin A (100nM) and genistein (10μM), prevented insulin from reducing the depolarization-evoked Ca²⁺ increase in rods. Their less active analogues, lavendustin B and daidzein, had similar effects. An insulin receptor-specific tyrosine kinase inhibitor, HNMPA-(AM)₃ (50μM), prevented insulin (30 nM) from reducing the depolarization-evoked Ca²⁺ increase in rods. The results suggest that insulin inhibits Ca²⁺ influx through voltage-dependent I_Ca in rod photoreceptors via tyrosine kinase activity.

Original language	English (US)
Pages (from-to)	947-951
Number of pages	5
Journal	Neuroreport
Volume	12
Issue number	5
DOIs	https://doi.org/10.1097/00001756-200104170-00017
State	Published - Apr 17 2001

All Science Journal Classification (ASJC) codes

General Neuroscience

Access to Document

10.1097/00001756-200104170-00017

Cite this

@article{a18875efe2f347068e41ed42e1ccde44,

title = "Insulin inhibits voltage-dependent calcium influx into rod photoreceptors",

abstract = "Insulin inhibits the ERG b-wave and modulates L-type calcium currents (ICa) in various preparations. We therefore examined insulin's effects on ICa and depolarization-evoked [Ca2+]i increases in rod photoreceptors. Insulin inhibited ICa and caused a dose-dependent reduction in the depolarization-evoked Ca2+ influx with an EC50 of 2.1 nM. Tyrosine kinase inhibitors, lavendustin A (100nM) and genistein (10μM), prevented insulin from reducing the depolarization-evoked Ca2+ increase in rods. Their less active analogues, lavendustin B and daidzein, had similar effects. An insulin receptor-specific tyrosine kinase inhibitor, HNMPA-(AM)3 (50μM), prevented insulin (30 nM) from reducing the depolarization-evoked Ca2+ increase in rods. The results suggest that insulin inhibits Ca2+ influx through voltage-dependent ICa in rod photoreceptors via tyrosine kinase activity.",

author = "Jr Stella and Bryson, {E. J.} and Thoreson, {W. B.}",

year = "2001",

month = apr,

day = "17",

doi = "10.1097/00001756-200104170-00017",

language = "English (US)",

volume = "12",

pages = "947--951",

journal = "Neuroreport",

issn = "0959-4965",

publisher = "Lippincott Williams and Wilkins",

number = "5",

}

TY - JOUR

T1 - Insulin inhibits voltage-dependent calcium influx into rod photoreceptors

AU - Stella, Jr

AU - Bryson, E. J.

AU - Thoreson, W. B.

PY - 2001/4/17

Y1 - 2001/4/17

N2 - Insulin inhibits the ERG b-wave and modulates L-type calcium currents (ICa) in various preparations. We therefore examined insulin's effects on ICa and depolarization-evoked [Ca2+]i increases in rod photoreceptors. Insulin inhibited ICa and caused a dose-dependent reduction in the depolarization-evoked Ca2+ influx with an EC50 of 2.1 nM. Tyrosine kinase inhibitors, lavendustin A (100nM) and genistein (10μM), prevented insulin from reducing the depolarization-evoked Ca2+ increase in rods. Their less active analogues, lavendustin B and daidzein, had similar effects. An insulin receptor-specific tyrosine kinase inhibitor, HNMPA-(AM)3 (50μM), prevented insulin (30 nM) from reducing the depolarization-evoked Ca2+ increase in rods. The results suggest that insulin inhibits Ca2+ influx through voltage-dependent ICa in rod photoreceptors via tyrosine kinase activity.

AB - Insulin inhibits the ERG b-wave and modulates L-type calcium currents (ICa) in various preparations. We therefore examined insulin's effects on ICa and depolarization-evoked [Ca2+]i increases in rod photoreceptors. Insulin inhibited ICa and caused a dose-dependent reduction in the depolarization-evoked Ca2+ influx with an EC50 of 2.1 nM. Tyrosine kinase inhibitors, lavendustin A (100nM) and genistein (10μM), prevented insulin from reducing the depolarization-evoked Ca2+ increase in rods. Their less active analogues, lavendustin B and daidzein, had similar effects. An insulin receptor-specific tyrosine kinase inhibitor, HNMPA-(AM)3 (50μM), prevented insulin (30 nM) from reducing the depolarization-evoked Ca2+ increase in rods. The results suggest that insulin inhibits Ca2+ influx through voltage-dependent ICa in rod photoreceptors via tyrosine kinase activity.

UR - http://www.scopus.com/inward/record.url?scp=0035901754&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035901754&partnerID=8YFLogxK

U2 - 10.1097/00001756-200104170-00017

DO - 10.1097/00001756-200104170-00017

M3 - Article

C2 - 11303766

AN - SCOPUS:0035901754

SN - 0959-4965

VL - 12

SP - 947

EP - 951

JO - Neuroreport

JF - Neuroreport

IS - 5

ER -

Insulin inhibits voltage-dependent calcium influx into rod photoreceptors

Abstract

All Science Journal Classification (ASJC) codes

Access to Document

Other files and links

Fingerprint

Cite this