May 2004
Volume 45, Issue 13
ARVO Annual Meeting Abstract  |   May 2004
The Absence of GABAC Receptor Mediated Inhibition Alters Retinal Dark Adaptation
Author Affiliations & Notes
  • P.J. DeMarco
    Dept Psychological and Brain Science,
    University of Louisville, Louisville, KY
    Louisville VA Medical Center, Louisville, KY
  • M.A. McCall
    Dept Psychological and Brain Science,
    Dept Ophthalmology and Visual Sciences,
    University of Louisville, Louisville, KY
  • Footnotes
    Commercial Relationships  P.J. DeMarco, None; M.A. McCall, None.
  • Footnotes
    Support  Department of Veterans Affairs; NSF ISBN 0079388
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 790. doi:
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      P.J. DeMarco, M.A. McCall; The Absence of GABAC Receptor Mediated Inhibition Alters Retinal Dark Adaptation . Invest. Ophthalmol. Vis. Sci. 2004;45(13):790.

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

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Abstract: : Purpose: To characterize the functional role of GABAC receptor–mediated inhibition in retinal adaptation. Methods: Full–field electroretinograms (ERG) were recorded from anesthetized GABAC null (Null) and wildtype (WT) mice. Stimuli were white light flashes, 10 ms in duration, with a 1 s inter–stimulus interval. Mice were prepared for recording under light–adapted conditions then plunged into darkness. The ERG was evoked by a constant intensity flash, presented at 1 min intervals for 15 min, then at 5 min intervals up to 50 min. Dark adaptation functions were constructed by plotting b–wave amplitude as a function of time in the dark. In addition, a double flash paradigm was used to assess rapid adaptation under both photopic and scotopic conditions. Two constant intensity 10 ms flashes were presented with inter–stimulus intervals that ranged from 10–500 ms. Rapid retinal adaptation was considered complete at the interval when the amplitude of the second b–wave recovered to match the amplitude of the first b–wave. Results: The ERG b–wave in WT mice grows in amplitude with increasing time in the dark and begins to plateau after 40 min. The function has two limbs, representing adaptation first by the cone pathway then by the rod pathway. In both WT and Null mice, the b–wave amplitude was similar up to 20 min, suggesting normal cone dark–adaptation. At around 20 min, the curve for Null mice shows a more shallow increase in b–wave amplitude, suggesting rod dark adaptation is slower in Null mice. The double flash experiment showed that the amplitude of the second b–wave was suppressed for inter–stimulus intervals of 100 ms or less, then recovers for longer inter–stimulus intervals. This trend was similar for both WT and Null mice under photopic and scotopic conditions. However, the b–wave amplitude in Null mice was significantly smaller than in WT mice under scotopic conditions, consistent with our dark adaptation results. Conclusions: Absence of GABAC receptor–mediated inhibition appears to play a role in dark adaptation within the rod system but not within the cone system. This effect may relate to the preponderance of GABAC receptors on rod bipolar cell axon terminals and may suggest a differential role of GABAC receptor–mediated inhibition between the two retinal pathways. Rapid retinal adaptation, measured at the level of the b–wave, does not appear to be altered in the absence of the GABAc receptor. These data further suggest that the GABAC receptor may be more influential in controlling slower adaptive processes within the rod pathway.

Keywords: retinal connections, networks, circuitry • inhibitory receptors • electroretinography: non–clinical 

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