Skip to main content

Thank you for visiting You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Article
  • Published:

Revival of light signalling in the postmortem mouse and human retina


Death is defined as the irreversible cessation of circulatory, respiratory or brain activity. Many peripheral human organs can be transplanted from deceased donors using protocols to optimize viability. However, tissues from the central nervous system rapidly lose viability after circulation ceases1,2, impeding their potential for transplantation. The time course and mechanisms causing neuronal death and the potential for revival remain poorly defined. Here, using the retina as a model of the central nervous system, we systemically examine the kinetics of death and neuronal revival. We demonstrate the swift decline of neuronal signalling and identify conditions for reviving synchronous in vivo-like trans-synaptic transmission in postmortem mouse and human retina. We measure light-evoked responses in human macular photoreceptors in eyes removed up to 5 h after death and identify modifiable factors that drive reversible and irreversible loss of light signalling after death. Finally, we quantify the rate-limiting deactivation reaction of phototransduction, a model G protein signalling cascade, in peripheral and macular human and macaque retina. Our approach will have broad applications and impact by enabling transformative studies in the human central nervous system, raising questions about the irreversibility of neuronal cell death, and providing new avenues for visual rehabilitation.

This is a preview of subscription content, access via your institution

Access options

Buy this article

Prices may be subject to local taxes which are calculated during checkout

Fig. 1: Postmortem decay and recovery of light-evoked retinal responses under in vivo and ex vivo conditions.
Fig. 2: Factors affecting recovered ERG b-wave amplitudes in postmortem mouse retinas.
Fig. 3: ERG b-wave is preserved in freshly obtained retinas from human donors after brain death.
Fig. 4: Comparison of phototransduction in rods and cones of the macula and periphery of freshly obtained retinas from human donors.

Similar content being viewed by others

Data availability

The data that support the findings of this study are available from G-Node at data are provided with this paper.


  1. Borjigin, J. et al. Surge of neurophysiological coherence and connectivity in the dying brain. Proc. Natl Acad. Sci. USA 110, 14432–14437 (2013).

    Article  ADS  CAS  PubMed  PubMed Central  Google Scholar 

  2. Cole, S. L. & Corday, E. Four-minute limit for cardiac resuscitation. J. Am. Med. Assoc. 161, 1454–1458 (1956).

    Article  CAS  PubMed  Google Scholar 

  3. Parnia, S., Waller, D. G., Yeates, R. & Fenwick, P. A qualitative and quantitative study of the incidence, features and aetiology of near death experiences in cardiac arrest survivors. Resuscitation 48, 149–156 (2001).

    Article  CAS  PubMed  Google Scholar 

  4. Vrselja, Z. et al. Restoration of brain circulation and cellular functions hours post-mortem. Nature 568, 336–343 (2019).

    Article  ADS  CAS  PubMed  PubMed Central  Google Scholar 

  5. Iyer, A. et al. Pathophysiological trends during withdrawal of life support: implications for organ donation after circulatory death. Transplantation 100, 2621–2629 (2016).

    Article  PubMed  Google Scholar 

  6. Donaldson, A. E. & Lamont, I. L. Biochemistry changes that occur after death: potential markers for determining post-mortem interval. PLoS ONE 8, e82011 (2013).

    Article  ADS  PubMed  PubMed Central  CAS  Google Scholar 

  7. Yu, D. Y. & Cringle, S. J. Oxygen distribution in the mouse retina. Invest. Ophthalmol. Vis. Sci. 47, 1109–1112 (2006).

    Article  PubMed  Google Scholar 

  8. Zhu, S. et al. Impact of euthanasia, dissection and postmortem delay on metabolic profile in mouse retina and RPE/choroid. Exp. Eye Res. 174, 113–120 (2018).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  9. Wu, J. Y. & Prentice, H. Role of taurine in the central nervous system. J. Biomed. Sci. 17, S1 (2010). Suppl. 1.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  10. Ingram, N. T., Fain, G. L. & Sampath, A. P. Elevated energy requirement of cone photoreceptors. Proc. Natl Acad. Sci. USA 117, 19599–19603 (2020).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  11. Cowan, C. S. et al. Cell types of the human retina and its organoids at single-cell resolution. Cell 182, 1623–1640.e1634 (2020).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  12. Wang, J. S. & Kefalov, V. J. An alternative pathway mediates the mouse and human cone visual cycle. Curr. Biol. 19, 1665–1669 (2009).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  13. Schnapf, J. L., Kraft, T. W. & Baylor, D. A. Spectral sensitivity of human cone photoreceptors. Nature 325, 439–441 (1987).

    Article  ADS  CAS  PubMed  Google Scholar 

  14. Kraft, T. W., Neitz, J. & Neitz, M. Spectra of human L cones. Vision Res. 38, 3663–3670 (1998).

    Article  CAS  PubMed  Google Scholar 

  15. Huang, J. C., Voaden, M. J. & Marshall, J. Survival of structure and function in postmortem rat and human retinas: rhodopsin regeneration, cGMP and the ERG. Curr. Eye Res. 9, 151–162 (1990).

    Article  CAS  PubMed  Google Scholar 

  16. Huang, J. C., Voaden, M. J., Marshall, J. & Kemp, C. M. Electrophysiologic characteristics of human and rat retinas in vitro. Doc. Ophthalmol. 76, 27–35 (1990).

    Article  CAS  PubMed  Google Scholar 

  17. Huang, J. C., Arden, G. B., Voaden, M. J. & Marshall, J. Survival of cone responses in postmortem human retina. Doc. Ophthalmol. 83, 91–96 (1993).

    Article  CAS  PubMed  Google Scholar 

  18. Kraft, T. W., Schneeweis, D. M. & Schnapf, J. L. Visual transduction in human rod photoreceptors. J. Physiol. 464, 747–765 (1993).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  19. Vinberg, F., Kolesnikov, A. V. & Kefalov, V. J. Ex vivo ERG analysis of photoreceptors using an in vivo ERG system. Vision Res. 101, 108–117 (2014).

    Article  PubMed  PubMed Central  Google Scholar 

  20. Nymark, S., Haldin, C., Tenhu, H. & Koskelainen, A. A new method for measuring free drug concentration: retinal tissue as a biosensor. Invest. Ophthalmol. Vis. Sci. 47, 2583–2588 (2006).

    Article  PubMed  Google Scholar 

  21. Weinstein, G. W., Hobson, R. R. & Dowling, J. E. Light and dark adaptation in the isolated rat retina. Nature 215, 134–138 (1967).

    Article  ADS  CAS  PubMed  Google Scholar 

  22. Winkler, B. S. The electroretinogram of the isolated rat retina. Vision Res. 12, 1183–1198 (1972).

    Article  CAS  PubMed  Google Scholar 

  23. Granit, R. The components of the retinal action potential in mammals and their relation to the discharge in the optic nerve. J. Physiol. 77, 207–239 (1933).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  24. Masland, R. H. & Ames, A. 3rd Dissociation of field potential from neuronal activity in the isolated retina: failure of the b-wave with normal ganglion cell response. J. Neurobiol. 6, 305–312 (1975).

    Article  CAS  PubMed  Google Scholar 

  25. Kim, H. M., Park, K. H. & Woo, S. J. Correlation of electroretinography components with visual function and prognosis of central retinal artery occlusion. Sci. Rep. 10, 12146 (2020).

    Article  ADS  CAS  PubMed  PubMed Central  Google Scholar 

  26. Reinhard, K. et al. Hypothermia promotes survival of ischemic retinal ganglion cells. Invest. Ophthalmol. Vis. Sci. 57, 658–663 (2016).

    Article  CAS  PubMed  Google Scholar 

  27. Mure, L. S., Vinberg, F., Hanneken, A. & Panda, S. Functional diversity of human intrinsically photosensitive retinal ganglion cells. Science 366, 1251–1255 (2019).

    Article  ADS  CAS  PubMed  PubMed Central  Google Scholar 

  28. Raeburn, C. D., Cleveland, J. C. Jr, Zimmerman, M. A. & Harken, A. H. Organ preconditioning. Arch. Surg. 136, 1263–1266 (2001).

    Article  CAS  PubMed  Google Scholar 

  29. Reinhard, K. & Munch, T. A. Visual properties of human retinal ganglion cells. PLoS ONE 16, e0246952 (2021).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  30. Soto, F. et al. Efficient coding by midget and parasol ganglion cells in the human retina. Neuron 107, 656–666.e655 (2020).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  31. Weinstein, G. W., Hobson, R. R. & Baker, F. H. Extracellular recordings from human retinal ganglion cells. Science 171, 1021–1022 (1971).

    Article  ADS  CAS  PubMed  Google Scholar 

  32. Robson, J. G., Saszik, S. M., Ahmed, J. & Frishman, L. J. Rod and cone contributions to the a-wave of the electroretinogram of the macaque. J. Physiol. 547, 509–530 (2003).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  33. Kuchenbecker, J. A., Greenwald, S. H., Neitz, M. & Neitz, J. Cone-isolating ON–OFF electroretinogram for studying chromatic pathways in the retina. J. Opt. Soc. Am. A 31, A208–A213 (2014).

    Article  ADS  Google Scholar 

  34. Yan, W. et al. Cell atlas of the human fovea and peripheral retina. Sci. Rep. 10, 9802 (2020).

    Article  ADS  CAS  PubMed  PubMed Central  Google Scholar 

  35. Lu, Y. et al. Single-cell analysis of human retina identifies evolutionarily conserved and species-specific mechanisms controlling development. Dev. Cell 53, 473–491.e479 (2020).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  36. Kling, A. et al. Functional organization of midget and parasol ganglion cells in the human retina. Preprint at (2020).

  37. Yi, W. et al. A single-cell transcriptome atlas of the aging human and macaque retina. Nat. Sci. Rev. 8, nwaa179 (2020).

    Article  CAS  Google Scholar 

  38. Fortenbach, C. R., Kessler, C., Peinado Allina, G. & Burns, M. E. Speeding rod recovery improves temporal resolution in the retina. Vision Res. 110, 57–67 (2015).

    Article  PubMed  PubMed Central  Google Scholar 

  39. Pepperberg, D. R. et al. Light-dependent delay in the falling phase of the retinal rod photoresponse. Vis. Neurosci. 8, 9–18 (1992).

    Article  CAS  PubMed  Google Scholar 

  40. Gross, O. P. & Burns, M. E. Control of rhodopsin’s active lifetime by arrestin-1 expression in mammalian rods. J. Neurosci. 30, 3450–3457 (2010).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  41. Krispel, C. M. et al. RGS expression rate-limits recovery of rod photoresponses. Neuron 51, 409–416 (2006).

    Article  CAS  PubMed  Google Scholar 

  42. Owsley, C. et al. Psychophysical evidence for rod vulnerability in age-related macular degeneration. Invest. Ophthalmol. Vis. Sci. 41, 267–273 (2000).

    CAS  PubMed  Google Scholar 

  43. Curcio, C. A., Medeiros, N. E. & Millican, C. L. Photoreceptor loss in age-related macular degeneration. Invest. Ophthalmol. Vis. Sci. 37, 1236–1249 (1996).

    CAS  PubMed  Google Scholar 

  44. Sinha, R. et al. Cellular and circuit mechanisms shaping the perceptual properties of the primate fovea. Cell 168, 413–426.e412 (2017).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  45. van Hateren, J. H. & Lamb, T. D. The photocurrent response of human cones is fast and monophasic. BMC Neurosci. 7, 34 (2006).

    Article  PubMed  PubMed Central  Google Scholar 

  46. Pearson, R. A. et al. Restoration of vision after transplantation of photoreceptors. Nature 485, 99–103 (2012).

    Article  ADS  CAS  PubMed  PubMed Central  Google Scholar 

  47. Wang, T. et al. Activation of rod input in a model of retinal degeneration reverses retinal remodeling and induces formation of functional synapses and recovery of visual signaling in the adult retina. J. Neurosci. 39, 6798–6810 (2019).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  48. Telias, M. et al. Retinoic acid induces hyperactivity, and blocking its receptor unmasks light responses and augments vision in retinal degeneration. Neuron 102, 574–586.e5 (2019).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  49. Jones, B. W. et al. Retinal remodeling and metabolic alterations in human AMD. Front. Cell. Neurosci. 10, 103 (2016).

    PubMed  PubMed Central  Google Scholar 

  50. Jones, B. W. et al. Retinal remodeling in human retinitis pigmentosa. Exp. Eye Res. 150, 149–165 (2016).

    Article  ADS  CAS  PubMed  PubMed Central  Google Scholar 

  51. Calvert, P. D. et al. Phototransduction in transgenic mice after targeted deletion of the rod transducin α-subunit. Proc. Natl Acad. Sci. USA 97, 13913–13918 (2000).

    Article  ADS  CAS  PubMed  PubMed Central  Google Scholar 

  52. Gurevich, L. & Slaughter, M. M. Comparison of the waveforms of the ON bipolar neuron and the b-wave of the electroretinogram. Vision Res. 33, 2431–2435 (1993).

    Article  CAS  PubMed  Google Scholar 

  53. Bolnick, D. A., Walter, A. E. & Sillman, A. J. Barium suppresses slow PIII in perfused bullfrog retina. Vision Res. 19, 1117–1119 (1979).

    Article  CAS  PubMed  Google Scholar 

  54. Sakami, S. et al. Probing mechanisms of photoreceptor degeneration in a new mouse model of the common form of autosomal dominant retinitis pigmentosa due to P23H opsin mutations. J. Biol. Chem. 286, 10551–10567 (2011).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  55. Marc, R. E., Murry, R. F. & Basinger, S. F. Pattern recognition of amino acid signatures in retinal neurons. J. Neurosci. 15, 5106–5129 (1995).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  56. Schindelin, J. et al. Fiji: an open-source platform for biological-image analysis. Nat. Methods 9, 676–682 (2012).

    Article  CAS  PubMed  Google Scholar 

  57. Lamb, T. D. & Pugh, E. N. Jr A quantitative account of the activation steps involved in phototransduction in amphibian photoreceptors. J. Physiol. 449, 719–758 (1992).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  58. Smith, N. P. & Lamb, T. D. The a-wave of the human electroretinogram recorded with a minimally invasive technique. Vision Res. 37, 2943–2952 (1997).

    Article  CAS  PubMed  Google Scholar 

Download references


This work was supported by National Institutes of Health (P30 EY014800), and an Unrestricted Grant from Research to Prevent Blindness to the Department of Ophthalmology and Visual Sciences, University of Utah. A.H. is supported by NIH/NCATS grant UL1 TR002550, NIH EY031706, the Daro Foundation, the A. C. Israel Foundation, the Warren Family Foundation, the Renaissance Charitable Foundation, The Rancho Santa Fe Foundation, the Money Arenz Foundation, the Considine Foundation, the Fonseca Foundation, the Pfeiffer Foundation, the Mericos Eye Institute, the Thomas and Audrey Pine Foundation and additional philanthropic funding. F.V. is supported by NIH grant EY031706, Research to Prevent Blindness/Dr. H. James and Carole Free Career Development Award, Diabetes Research Connection, and International Retinal Research Foundation. S.B. is supported by ARVO Foundation for Eye Research EyeFind research grant. B.W.J. is supported by the National Institutes of Health (R01 EY015128, R01 EY028927) and the National Science Foundation (2014862). S.P. is supported by the National Institutes of Health (R01s: CA236352, DK115214, DK118278), Department of Defense (W81XWH1810645), and Wu-Tsai Human Performance Alliance and the Joe and Clara Tsai Foundation. L.S.M. is supported by Velux Stiftung. Figure schematics were made with resources from We thank J. Dessert for producing the surgical donation and transportation illustrations in Fig. 3a; J. R. Allen for the fusion 360 model of the ex vivo ERG specimen holder in Extended Data Fig. 3; T. Neikirk, a member of the Hanneken laboratory, for providing technical support and assistance; H. Calligaro, a member of the Panda laboratory, for useful discussions of some of the most recent human retina experiments; C. Faulkner and J. Perlmutter for providing non-human primate eyes; the Utah Lions Eye Bank, Lifesharing and the San Diego Eye bank for providing human donor eyes. Finally, we are deeply grateful to those who donated their eyes, and their legal representatives who accommodated the surgical team’s effort to procure the eyes.

Author information

Authors and Affiliations



A.H. and F.V. conceived, organized and supervised the project. S.B. carried out and analysed mouse in vivo ERG and low-oxygen ex vivo ERG experiments. F.A. collected and analysed death-to-enucleation delay and low pH mouse ex vivo ERG data and carried out mouse immunohistochemistry staining and imaging. B.W.J. carried out and analysed CMP staining. F.A. and F.V. collected and analysed human research donor data. A.H. recovered the organ donor eyes. F.A., F.V. and L.S.M. acquired and analysed human organ donor data. F.V. acquired and analysed macaque data. F.A. and F.V. prepared the figures. F.A., A.H., S.P. and F.V. wrote the manuscript. All authors discussed and commented on the data.

Corresponding authors

Correspondence to Anne Hanneken or Frans Vinberg.

Ethics declarations

Competing interests

The authors declare no competing interests.

Peer review

Peer review information

Nature thanks Michael Gorin, Andrew Huberman and the other, anonymous, reviewers for their contribution to the peer review of this work.

Additional information

Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Extended data figures and tables

Extended Data Fig. 1 Changes after 45 min death-to-enucleation delay to metabolites related to cell health and synaptic signaling.

Example RGB maps of CMP staining of metabolites in the immediately fixed vs. 45-minute postmortem wild-type retina (a). τQE (Taurine, Glutamine, Glutamate) → RGB for both immediate and 45 min PM retinas. The density maps for each metabolite are also shown (greyscale). Scale bar represents 50 μm. Histograms of the mean levels of Taurine, Glutamine and Glutamate measured in retinas either after immediate enucleation (black) or 45 min enucleation delay (red, b), according to masked cell populations (n = 3 retinas from 3 animals). Data are presented as averages (lines) ± SEM (shaded areas).

Extended Data Fig. 2 Phototransduction sensitivity and kinetics in relation to enucleation delay.

Example plot showing how dim flash response sensitivity is calculated (a). Responses normalized to maximal response of retina plotted against the intensity of light stimulus, curve fits Naka-Rushton function (Eq. 2) to amplitude data, dim flash sensitivity is defined as response amplitude divided by Rmax at constant intensity producing ~20% of the maximal response amplitude. Dim flash sensitivities of retinas from wild-type mouse retinas with different enucleation delays (b), and I1/2 values from retinas of wild-type mice with different enucleation delays (c). Example response plot showing how I1/2 was obtained (d), responses of retina to each intensity presented is plotted and a Naka-Rushton fit applied to the plot. I1/2 is the intensity required to produce half the maximal response size. Amplification constant plotted against enucleation delay for each retina (e). Time-to-peak (tp) and integral (Ti, inset) of dim responses for each retina plotted against the enucleation delay (f, *** indicates p < 0.001 compared to 0min). Exact p values: tp: 0 vs 90 min p = 0.0002, 0 vs 120 min p = 0.002, 0 vs 180 min p = 0.001, Ti: 0 vs 90 min p = 0.002, 0 vs 120 min p = 0.0007, 0 vs 180 min p = 0.01). Example dim flash response showing how time-to-peak (tp) and integration time (Ti) was calculated (g). Time-to-peak is the time from light stimulus onset to the peak of the dim flash response. Integral (Ti) is the area under the dim flash response curve (orange shaded area), divided by the response amplitude. Light stimulus is indicated with a shaded yellow area. For all plots, bar height indicates mean, error bars represent ± SEM. All comparisons are one-way ANOVA with Holm-Bonferroni means comparisons. (DF: 35 for all comparisons, F values: Ti = 8.4, tp = 5.8, Dim flash sensitivity = 2.0, Amplification constant = 1.6, I1/2 : 2.2).

Extended Data Fig. 3 Drawings of ex vivo ERG specimen holder for CNC machining from polycarbonate.

(exported from Fusion 360, Autodesk, used to design the specimen holder for CNC machining). Retina samples are placed on the dome (shaded in blue in b). The dome has electrode channel with 0.5–2 mm diameter that determines the recording area. O-ring (a, black shading; b, pink shading) minimizes shunt currents to improve signal-to-noise ratio (SNR).

Extended Data Fig. 4 Comparison of freshly enucleated Macaque retina, and human organ and research donor maculas with longer enucleation delays.

Light responses of macular cones from freshly enucleated macaque (a, hatched squares, n = 5 maculae, from 3 animals) human DCD donor (b, filled triangles, top trace, n = 5 maculae from 3 donors) and research donor eyes (b, crosses lower trace, n = 23 maculae from 17 donors). (c) The maximal response obtained from maculae from each tissue type plotted against enucleation delay. Inset shows Ln of Rmax from each macula, and linear fit in red with decay (τ = 74 min). (d) Example of how sensitivity, S (1/I½), is calculated. Macular responses to different light intensities were plotted and a Hill curve fitted (see Eq. 3 in Methods) to determine the intensity required to produce a half-maximal response size. (e) Sensitivities of each macula plotted against enucleation delay, linear fit in red (no significant correlation between delay and S, ANOVA, DF =24, F value = 3.9, p = 0.06).

Extended Data Fig. 5 Contributing factors to the quality of light-evoked responses from human postmortem research donor retinas.

(a) Histogram of research donor ages, with numbers of donors represented within the bars. (b) Histogram of the primary cause of death of donors as noted on tissue donor forms. (c) The maximal response obtained from each donor eye plotted against donor age, with linear fit showing a positive correlation (n = 23 maculae, Pearson’s r = 0.61, adjusted R2 = 0.37) (d) Average maximal amplitude obtained from each research donor according to the primary cause of death (Stroke: squares, n = 2 donors, ACE: circles, n = 4 donors, Sepsis: triangles, n = 7 donors), data are averages of responses obtained from each individual donor, with mean presented as a solid line. Maculae that did not produce any detectable responses were included as a response size of 0 µV. Donor information (e) for a single donor (donor #8) in which ex vivo ERG ON-bipolar cell responses were recorded to flash intensities of 29–32,500 photons µm−2(f). Yellow bar indicates the onset of flash stimuli.

Extended Data Fig. 6 Decay of cone photoreceptor and bipolar cell function in relation to the enucleation delay in Gnat1−/− mice.

(a) The Rmax of mouse cone photoreceptors (black circle) and bipolar cells (red circle) plotted as a function of enucleation delay, normalized to maximal response obtained with 0 min enucleation delay. Smooth traces plot exponential decay function fitted to mean data. Inset plots natural log amplitude data for individual retinas (τ = 53 min for photoreceptors, τ = 35 min for bipolar cells), and linear fit (Photoreceptor fit: Pearson’s r = −0.851 with adj. R2 = 0.704, Bipolar cell fit: Pearson’s r = 0.905 with adj R2 = 0.819). Sensitivity of retinas at different enucleation delays (b, 1/I1/2), Pearson’s r = 0.52 with adj. R2 = 0.27. For all plots, n (retinas, animals) is 0min = 7, 45 min = 5, 120 min = 3, responses from individual retinas are plotted as hollow circles.

Extended Data Fig. 7 Double-flash responses allow the isolation of cone responses from rod in both human macula (a) and periphery (b).

Representative responses from human donor macular (a, black) and peripheral (b, red) punches to double-flash light stimuli to isolate cone responses. Light flashes are indicated with yellow shading, rod saturating flash intensity was ~25,000, cone stimulating intensities used were 2800–147,000 photons (560 nm) µm−2.

Extended Data Fig. 8 Comparison of Human Macular and Peripheral Cone sensitivity and kinetics.

Dim flash response time-to-peak (at intensity producing response size 15–20% of maximal retina response in ms) recorded from human macular and peripheral cone responses (c), individual responses are shown as diamonds, with line indicating mean. The average dim flash photoreceptor response normalized to maximal response recorded from each retina, plotted against time (d). Graph line shows average response with shaded area showing ± SEM.

Extended Data Fig. 9 Determination of dominant time constant (τD) for macaque cones.

Representative responses to flashes of light ranging from 220 to 183,000 photons (500 nm) µm−2 from a macular (a) and peripheral (c) sample recorded using ex vivo ERG. A rod-saturating pre-flash (15,000 photons µm−2 at 500 nm) was used to isolate cones in peripheral samples. Saturation times (Tsat) measured at 50% recovery (example red dashed line in a, c) plotted as a function of logarithmic light flash intensity (in photons µm−2) for induvial macular (b) and peripheral samples (d). e. Log response amplitudes plotted against light intensities in macaque maculae (black) and peripheral retina punches (red) with Hill function fits (Eq. 3 in Methods) . n = 5 macular and n = 7 peripheral punches from 3 animals. (f) Table of statistics for slopes in (b, d), i.e. τD, mean ± SEM.

Supplementary information

Supplementary Tables

Supplementary Tables 1–6.

Reporting Summary

Source data

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Abbas, F., Becker, S., Jones, B.W. et al. Revival of light signalling in the postmortem mouse and human retina. Nature 606, 351–357 (2022).

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI:

This article is cited by


By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate.


Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing