December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Immunolocalization of Melatonin Receptor Subtypes in Photoreceptors and Inner Retinal Neurons of Xenopus laevis Retina
Author Affiliations & Notes
  • AF Wiechmann
    Departments of Cell Biology and Ophthalmology Univ Oklahoma Hlth Sci Center Oklahoma City OK
  • K Aoki
    Department of Cell Biology
    University of Oklahoma Hlth Sci Center Oklahoma City OK
  • MJ Vrieze
    Department of Cell Biology
    University of Oklahoma Hlth Sci Center Oklahoma City OK
  • CR Wirsig-Wiechmann
    Departments of Cell Biology and Zoology
    University of Oklahoma Hlth Sci Center Oklahoma City OK
  • Footnotes
    Commercial Relationships   A.F. Wiechmann, None; K. Aoki, None; M.J. Vrieze, None; C.R. Wirsig-Wiechmann, None. Grant Identification: Support: OCAST Grant HR01-149
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 1362. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      AF Wiechmann, K Aoki, MJ Vrieze, CR Wirsig-Wiechmann; Immunolocalization of Melatonin Receptor Subtypes in Photoreceptors and Inner Retinal Neurons of Xenopus laevis Retina . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1362.

      Download citation file:


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

      ×
  • Supplements
Abstract

Abstract: : Purpose: The hormone melatonin is an output signal of the endogenous circadian clock in retinal photoreceptors, and may act as a paracrine and/or intracrine neurohormone by binding to specific receptors in the eye. The goal of this study was to identify the retinal cells that express the Mel1a and Mel1c receptor subtype proteins, and to confirm the presence of receptor expression in photoreceptor cells by measuring photoreceptor membrane currents in response to applied melatonin. Methods: Sections of adult Xenopus laevis neural retina and retinal pigment epithelium (RPE) were analyzed by immunocytochemistry and confocal microscopy, using antibodies prepared against specific sequences of the Mel1a and Mel1c receptor proteins. Other retinal cell markers that label dopaminergic amacrine cells (TOH) and GABA-ergic (GAD) amacrine cells were used in double-label experiments. To test the hypothesis that functional melatonin receptors are present on photoreceptor cells, rod photoreceptors in retinal slice preparations were analyzed by whole cell patch clamp recording. The cells were voltage clamped at -60 mV and a series of voltage steps were applied in the presence or absence of 100 nM melatonin, or vehicle control solution. Results: The distribution of Mel1a and Mel1c receptor subtype immunoreactivity was similar in some regards, since the two subtypes were co-localized in the inner plexiform layer (IPL). However, The Mel1c showed a much higher intensity of immunoreactivity in the photoreceptor cells, and the Mel1a subtype did not reveal any photoreceptor labeling. The Mel1c antibody, but not the Mel1a, labeled ganglion cell soma. While both receptor subtypes were localized to the outer plexiform layer (OPL), they did not appear to co-localize to the identical cell types. Melatonin reduced the magnitude of the inward current in most rod cells studied, and also suppressed the overall magnitude of the rod membrane current in retinal slices. Conclusion: The Mel1a and Mel1c receptor proteins are present in the Xenopus laevis retina, and their distribution in the photoreceptors and inner retina is very similar to that reported in the human retina, and supports the previous report that melatonin receptor RNA is localized to photoreceptors. The melatonin-induced change in membrane currents in rod cells supports the concept that photoreceptor cells are direct targets for melatonin.

Keywords: 465 melatonin • 517 photoreceptors • 349 circadian rhythms 
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×