June 2013
Volume 54, Issue 15
Free
ARVO Annual Meeting Abstract  |   June 2013
Adaptive acceleration in mouse rods is mediated by slow feedback via guanylate cyclase activating proteins
Author Affiliations & Notes
  • Marie Burns
    Center for Neuroscience, Univ of California-Davis, Davis, CA
    Cell Biology and Human Anatomy, Univ of California-Davis, Davis, CA
  • Owen Gross
    Center for Neuroscience, Univ of California-Davis, Davis, CA
  • Claudia Krispel
    Ophthalmology & Vision Science, Univ of California-Davis, Davis, CA
    Wilmer Eye Institute, Johns Hopkins Hospital, Baltimore, MD
  • Footnotes
    Commercial Relationships Marie Burns, None; Owen Gross, None; Claudia Krispel, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 2457. doi:
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      Marie Burns, Owen Gross, Claudia Krispel; Adaptive acceleration in mouse rods is mediated by slow feedback via guanylate cyclase activating proteins. Invest. Ophthalmol. Vis. Sci. 2013;54(15):2457.

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

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Abstract

Purpose: In retinal photoreceptors, adaptation to steady background light produces several specific changes in phototransduction biochemistry and the incremental flash response. A long-lasting form of adaptation termed “adaptive acceleration” (AA) has been found to shorten responses for many tens of seconds following the offset of saturating light, but the mechanism and functional significance of this form of adaptation has been unknown.

Methods: Suction electrodes were used to record the outer segment membrane current of individual rods of mice before, during, and after an adapting stimulus (500 nm light) that varied both in intensity and duration. Adaptive acceleration was probed using brief (10 ms) flashes of light of fixed intensity. The dominant time constant of recovery was probed using saturating flashes whose intensity varied 2-8 fold in the period immediately before and after the adapting light, and by measuring the time that these flash responses remained in saturation.

Results: As described previously, AA was easily induced using steady light that suppressed the rod’s circulating current. The induction of AA required extended periods of response saturation, with an onset time constant of 35 s, and faded with a time constant of ~80 s. Analysis of a sequence of saturating flash responses immediately after the adapting light offset revealed that, contrary to an earlier report, AA was not associated with the shortening of the dominant time constant of recovery, indicating that it is not caused by acceleration of GTPase activity. Indeed, rods that overexpressed the RGS9 complex or which lacked several other targets for adaptation, including recoverin, showed the normal induction and offset features of AA. However, AA was completely abolished in the rods of mice lacking guanylate cyclase activating proteins, or GCAPs. Furthermore, AA improved the flicker response properties of wild-type rods, but not in rods lacking GCAPs.

Conclusions: GCAPs have previously been described to play a role in setting the single photon response amplitude and in preventing saturation in steady light (Mendez et al., 2001; Burns et al., 2002; Gross et al 2012). Our findings in the current study suggest that GCAPs also mediate a longer-lasting change in guanylate cyclase activity that improves the temporal resolution of the rods following a bright steady light.

Keywords: 648 photoreceptors  
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