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This Article Full Text Full Text (PDF) All Versions of this Article: 575/2/507    most recent jphysiol.2006.108027v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Cameron, A. M. Articles by Lamb, T. D. Search for Related Content PubMed PubMed Citation Articles by Cameron, A. M. Articles by Lamb, T. D. Related Collections Neuroscience

¹ Division of Neuroscience, John Curtin School of Medical Research
² ARC Centre of Excellence in Vision Science, Australian National University, Canberra, ACT 0200, Australia
³ Physiological Laboratory, University of Cambridge, Downing Street, Cambridge CB2 3EG, UK

To examine the dark adaptation of human rod bipolar cells in vivo, we recorded ganzfeld ERGs to (a) a family of flashes of increasing intensity, (b) dim test flashes presented on a range of background intensities, and (c) dim test flashes presented before, and up to 40 min after, exposure to intense illumination eliciting bleaches from a few per cent to near total. The dim flash ERG was characterized by a prominent b-wave response generated principally by rod bipolar cells. In the presence of background illumination the response reached peak earlier and desensitized according to Weber's Law. Following bleaching exposures, the response was initially greatly desensitized, but thereafter recovered slowly with time. For small bleaches, the desensitization was accompanied by acceleration, in much the same way as for real light. Following a near-total bleach, the response was unrecordable for >10 min, but after 23 min half-maximal sensitivity was reached, and full sensitivity was restored between 35 and 40 min. With smaller bleaches, recovery commenced earlier. We converted the post-bleach measurements of desensitization into ‘equivalent background intensities’ using a Crawford transformation. Across the range of bleaching levels, the results were described by a prominent ‘S2’ component (0.24 decades min^–1) together with a smaller and slower ‘S3’ component (0.06 decades min^–1), as is found for dark adaptation of the scotopic visual system. We attribute the S2 component to the presence of unregenerated opsin, and we speculate that the S3 component results from ion channel closure by all-trans retinal.

(Received 21 February 2006; accepted after revision 12 June 2006; first published online 15 June 2006)
Corresponding authors A. M. Cameron and T. D. Lamb: Division of Neuroscience, John Curtin School of Medical Research, Australian National University, Canberra, ACT 0200, Australia. Email: allison.cameron{at}anu.edu.au and trevor.lamb{at}anu.edu.au