Voltage-dependent calcium channel CaV1.3 subunits regulate the light peak of the electroretinogram

Jiang Wu, Alan D Marmorstein, Jörg Striessnig, Neal S. Peachey

Research output: Contribution to journalArticle

43 Citations (Scopus)

Abstract

In response to light, the mouse retinal pigment epithelium (RPE) generates a series of slow changes in potential that are referred to as the c-wave, fast oscillation (FO), and light peak (LP) of the electroretinogram (ERG). The LP is generated by a depolarization of the basolateral RPE plasma membrane by the activation of a calcium-sensitive chloride conductance. We have previously shown that the LP is reduced in both mice and rats by nimodipine, which blocks voltage-dependent calcium channels (VDCCs) and is abnormal in lethargic mice, carrying a null mutation in the calcium channel β4 subunit. To define the α1 subunit involved in this process, we examined mice lacking CaV1.3. In comparison with wild-type (WT) control littermates, LPs were reduced in CaV1.3-/- mice. This pattern matched closely with that previously noted in lethargic mice, confirming a role for VDCCs in regulating the signaling pathway that culminates in LP generation. These abnormalities do not reflect a defect in rod photoreceptor activity, which provides the input to the RPE to generate the c-wave, FO, and LP, because ERG a-waves were comparable in WT and CaV1.3 -/- littermates. Our results identify CaV1.3 as the principal pore-forming subunit of VDCCs involved in stimulating the ERG LP.

Original languageEnglish (US)
Pages (from-to)3731-3735
Number of pages5
JournalJournal of Neurophysiology
Volume97
Issue number5
DOIs
StatePublished - May 2007
Externally publishedYes

Fingerprint

Calcium Channels
Light
Retinal Pigment Epithelium
Retinal Rod Photoreceptor Cells
Nimodipine
Calcium Chloride
Cell Membrane
Mutation

ASJC Scopus subject areas

  • Physiology
  • Neuroscience(all)

Cite this

Voltage-dependent calcium channel CaV1.3 subunits regulate the light peak of the electroretinogram. / Wu, Jiang; Marmorstein, Alan D; Striessnig, Jörg; Peachey, Neal S.

In: Journal of Neurophysiology, Vol. 97, No. 5, 05.2007, p. 3731-3735.

Research output: Contribution to journalArticle

@article{62d9f8f980144ec790c96c0ada43808c,
title = "Voltage-dependent calcium channel CaV1.3 subunits regulate the light peak of the electroretinogram",
abstract = "In response to light, the mouse retinal pigment epithelium (RPE) generates a series of slow changes in potential that are referred to as the c-wave, fast oscillation (FO), and light peak (LP) of the electroretinogram (ERG). The LP is generated by a depolarization of the basolateral RPE plasma membrane by the activation of a calcium-sensitive chloride conductance. We have previously shown that the LP is reduced in both mice and rats by nimodipine, which blocks voltage-dependent calcium channels (VDCCs) and is abnormal in lethargic mice, carrying a null mutation in the calcium channel β4 subunit. To define the α1 subunit involved in this process, we examined mice lacking CaV1.3. In comparison with wild-type (WT) control littermates, LPs were reduced in CaV1.3-/- mice. This pattern matched closely with that previously noted in lethargic mice, confirming a role for VDCCs in regulating the signaling pathway that culminates in LP generation. These abnormalities do not reflect a defect in rod photoreceptor activity, which provides the input to the RPE to generate the c-wave, FO, and LP, because ERG a-waves were comparable in WT and CaV1.3 -/- littermates. Our results identify CaV1.3 as the principal pore-forming subunit of VDCCs involved in stimulating the ERG LP.",
author = "Jiang Wu and Marmorstein, {Alan D} and J{\"o}rg Striessnig and Peachey, {Neal S.}",
year = "2007",
month = "5",
doi = "10.1152/jn.00146.2007",
language = "English (US)",
volume = "97",
pages = "3731--3735",
journal = "Journal of Neurophysiology",
issn = "0022-3077",
publisher = "American Physiological Society",
number = "5",

}

TY - JOUR

T1 - Voltage-dependent calcium channel CaV1.3 subunits regulate the light peak of the electroretinogram

AU - Wu, Jiang

AU - Marmorstein, Alan D

AU - Striessnig, Jörg

AU - Peachey, Neal S.

PY - 2007/5

Y1 - 2007/5

N2 - In response to light, the mouse retinal pigment epithelium (RPE) generates a series of slow changes in potential that are referred to as the c-wave, fast oscillation (FO), and light peak (LP) of the electroretinogram (ERG). The LP is generated by a depolarization of the basolateral RPE plasma membrane by the activation of a calcium-sensitive chloride conductance. We have previously shown that the LP is reduced in both mice and rats by nimodipine, which blocks voltage-dependent calcium channels (VDCCs) and is abnormal in lethargic mice, carrying a null mutation in the calcium channel β4 subunit. To define the α1 subunit involved in this process, we examined mice lacking CaV1.3. In comparison with wild-type (WT) control littermates, LPs were reduced in CaV1.3-/- mice. This pattern matched closely with that previously noted in lethargic mice, confirming a role for VDCCs in regulating the signaling pathway that culminates in LP generation. These abnormalities do not reflect a defect in rod photoreceptor activity, which provides the input to the RPE to generate the c-wave, FO, and LP, because ERG a-waves were comparable in WT and CaV1.3 -/- littermates. Our results identify CaV1.3 as the principal pore-forming subunit of VDCCs involved in stimulating the ERG LP.

AB - In response to light, the mouse retinal pigment epithelium (RPE) generates a series of slow changes in potential that are referred to as the c-wave, fast oscillation (FO), and light peak (LP) of the electroretinogram (ERG). The LP is generated by a depolarization of the basolateral RPE plasma membrane by the activation of a calcium-sensitive chloride conductance. We have previously shown that the LP is reduced in both mice and rats by nimodipine, which blocks voltage-dependent calcium channels (VDCCs) and is abnormal in lethargic mice, carrying a null mutation in the calcium channel β4 subunit. To define the α1 subunit involved in this process, we examined mice lacking CaV1.3. In comparison with wild-type (WT) control littermates, LPs were reduced in CaV1.3-/- mice. This pattern matched closely with that previously noted in lethargic mice, confirming a role for VDCCs in regulating the signaling pathway that culminates in LP generation. These abnormalities do not reflect a defect in rod photoreceptor activity, which provides the input to the RPE to generate the c-wave, FO, and LP, because ERG a-waves were comparable in WT and CaV1.3 -/- littermates. Our results identify CaV1.3 as the principal pore-forming subunit of VDCCs involved in stimulating the ERG LP.

UR - http://www.scopus.com/inward/record.url?scp=34447302337&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34447302337&partnerID=8YFLogxK

U2 - 10.1152/jn.00146.2007

DO - 10.1152/jn.00146.2007

M3 - Article

VL - 97

SP - 3731

EP - 3735

JO - Journal of Neurophysiology

JF - Journal of Neurophysiology

SN - 0022-3077

IS - 5

ER -