May 2007
Volume 48, Issue 13
ARVO Annual Meeting Abstract  |   May 2007
Role of Voltage Dependent Calcium Channel 1D Subunits in the ERG Light Peak Pathway
Author Affiliations & Notes
  • J. Wu
    Ophthalmic Research, Cole Eye Institute of Cleveland Clinic Foundation, Cleveland, Ohio
  • A. D. Marmorstein
    Department of Ophthalmology, University of Arizona, Tucson, Arizona
  • Jö. Striessnig
    Abteilung Pharmakologie und Toxikologie, Institut fur Pharmazie, Universitat Innsbruck, Innsbruck, Austria
  • N. S. Peachey
    Ophthalmic Research, Cole Eye Institute of Cleveland Clinic Foundation, Cleveland, Ohio
    Research Service, Cleveland VA Medical Center, Cleveland, Ohio
  • Footnotes
    Commercial Relationships J. Wu, None; A.D. Marmorstein, None; J. Striessnig, None; N.S. Peachey, None.
  • Footnotes
    Support NEI (R01EY14465; R01EY13160; R24EY15638), Austrian Science Fund grant P17159 HIGHWIRE EXLINK_ID="48:5:1521:1" VALUE="P17159" TYPEGUESS="GEN, PIRDB, SPROT" /HIGHWIRE , the Macular Vision Research Foundation, the Department of Veterans Affairs, and Research to Prevent Blindness.
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 1521. doi:
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    • Get Citation

      J. Wu, A. D. Marmorstein, Jö. Striessnig, N. S. Peachey; Role of Voltage Dependent Calcium Channel 1D Subunits in the ERG Light Peak Pathway. Invest. Ophthalmol. Vis. Sci. 2007;48(13):1521.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose:: The electroretinogram (ERG) provides a convenient non-invasive means to monitor the functional status of the neural retina and of the retinal pigment epithelium (RPE), an epithelial layer that plays many important roles in maintaining normal retinal function. The RPE generates three major ERG components, the slowest of which is termed the light peak (LP) and is generated on the basal surface. Prior studies indicate a prominent role of voltage dependent calcium channels (VDCCs) in LP generation [1]. First, this component is selectively reduced by nimodipine. Second, the LP is selectively reduced in lethargic mice, which harbor a loss of function mutation in the VDCC ß4 subunit. Here we demonstrate that the CaV1.3 subunit is also involved.

Methods:: After overnight dark adaptation, mice were anesthetized, the pupils were dilated, and dc-ERGs were recorded from the corneal surface in response to 7-minute duration stimuli, the intensity of which was controlled with neutral density filters [2]. In a separate recording session, strobe flash stimuli were used to evaluate function of rod photoreceptors, the activity of which activates the RPE.

Results:: In comparison to WT littermates, LPs of CaV1.3-/- mice were significantly decreased in amplitude. This reduction does not reflect an abnormality in retinal function, as ERG a-waves were normal.

Conclusions:: These results demonstrate that LP generation depends upon VDCC activation. This observation, coupled with the finding that mice lacking bestrophin generate normal or larger than normal LPs [1] indicate the LP is generated by an as-yet unidentified calcium sensitive chloride channel located on the basal membrane of RPE cells. The activity of this channel is modulated by VDCC activity, which is in turn modulated by bestrophin. [1] Marmorstein et al., J Gen Physiol 2006;127:57 [2] Wu et al., J Neurophysiol 2004;91:1134

Keywords: electroretinography: non-clinical • retinal pigment epithelium • ion channels 

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