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      ON-OFF Interactions in the Retina: Role of Glycine and GABA

      research-article
      Author(s): *
      Publication date (Electronic):
      Journal: Current Neuropharmacology
      Publisher: Bentham Science Publishers
      Keywords: Bipolar cells, electroretinogram, GABA, ganglion cells, glycine, ON-OFF interactions, retina

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          Abstract

          In the vertebrate retina, visual signals are segregated into parallel ON and OFF pathways, which provide information for light increments and decrements. The segregation is first evident at the level of the ON and OFF bipolar cells and it apparently remains as signals propagate to higher brain visual centers. A fundamental question in visual neuroscience is how these two parallel pathways function: are they independent from each other or do they interact somehow? In the latter case, what kinds of mechanisms are involved and what are the consequences from this cross-talk? This review summarizes current knowledge about the types of interactions between the ON and OFF channels in nonmammalian and mammalian retina. Data concerning the ON-OFF interactions in distal retina revealed by recording of single bipolar cell activity and electroretinographic ON (b-wave) and OFF (d-wave) responses are presented. Special emphasis is put on the ON-OFF interactions in proximal retina and their dependence on the state of light adaptation in mammalian retina. The involvement of the GABAergic and glycinergic systems in the ON-OFF crosstalk is also discussed.

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          2-amino-4-phosphonobutyric acid: a new pharmacological tool for retina research.

          Malcolm M. Slaughter, Michael R. Miller (1981)
          Information processing in the vertebrate retina occurs in two separate channels known as ON and OFF channels. When intracellular electrophysiological recordings were obtained from the perfused retina-eyecup preparation of the mud-puppy (Necturus maculosus), the addition of 2-amino-4-phosphonobutyric acid to the bathing medium blocked all responses in the ON channel but left intact the OFF responses including OFF ganglion cell discharge. 2-Amino-4-phosphonobutyric acid blocks the light response of the ON bipolar cell by mimicking the endogenous photoreceptor transmitter.
          Article 0 comments Cited 72 times – based on 0 reviews     Review now
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            B-wave of the electroretinogram. A reflection of ON bipolar cell activity

            MM Slaughter, RA Stockton (1989)
            Light-evoked intraretinal field potentials (electroretinogram, ERG) have been measured simultaneously with extracellular potassium fluxes in the amphibian retina. The application of highly selective pharmacologic agents permitted us to functionally isolate various classes of retinal neurons. It was found that: (a) application of APB (2-amino-4-phosphonobutyrate), which has previously been shown to selectively abolish the light responsiveness of ON bipolar cells, causes a concomitant loss of the ERG b-wave and ON potassium flux. (b) Conversely, PDA (cis 2,3-piperidine-dicarboxylic acid) or KYN (kynurenic acid), which have been reported to suppress the light responses of OFF bipolar, horizontal, and third-order retinal neurons, causes a loss of the ERG d-wave as well as OFF potassium fluxes. The b- wave and ON potassium fluxes, however, remain undiminished. (c) NMA (N- methyl-DL-aspartate) or GLY (glycine), which have been reported to suppress the responses of third-order neurons, do not diminish the b- or d-waves, nor the potassium fluxes at ON or OFF. This leads to the conclusion that the b-wave of the ERG is a result of the light-evoked depolarization of the ON bipolar neurons. This experimental approach has resulted in two further conclusions: (a) that the d-wave is an expression of OFF bipolar and/or horizontal cell depolarization at the termination of illumination and (b) that light-induced increases in extracellular potassium concentration in both the inner (proximal) and outer (distal) retina are the result of ON bipolar cell depolarization.
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              Mutations in NYX, encoding the leucine-rich proteoglycan nyctalopin, cause X-linked complete congenital stationary night blindness.

              Jesper N Bech, R Weleber, R Sparkes … (2000)
              During development, visual photoreceptors, bipolar cells and other neurons establish connections within the retina enabling the eye to process visual images over approximately 7 log units of illumination. Within the retina, cells that respond to light increment and light decrement are separated into ON- and OFF-pathways. Hereditary diseases are known to disturb these retinal pathways, causing either progressive degeneration or stationary deficits. Congenital stationary night blindness (CSNB) is a group of stable retinal disorders that are characterized by abnormal night vision. Genetic subtypes of CSNB have been defined and different disease actions have been postulated. The molecular bases have been elucidated in several subtypes, providing a better understanding of the disease mechanisms and developmental retinal neurobiology. Here we have studied 22 families with 'complete' X-linked CSNB (CSNB1; MIM 310500; ref. 4) in which affected males have night blindness, some photopic vision loss and a defect of the ON-pathway. We have found 14 different mutations, including 1 founder mutation in 7 families from the United States, in a novel candidate gene, NYX. NYX, which encodes a glycosylphosphatidyl (GPI)-anchored protein called nyctalopin, is a new and unique member of the small leucine-rich proteoglycan (SLRP) family. The role of other SLRP proteins suggests that mutant nyctalopin disrupts developing retinal interconnections involving the ON-bipolar cells, leading to the visual losses seen in patients with complete CSNB.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Curr Neuropharmacol
                Journal ID (iso-abbrev): Curr Neuropharmacol
                Journal ID (publisher-id): CN
                Title: Current Neuropharmacology
                Publisher: Bentham Science Publishers
                ISSN (Print): 1570-159X
                ISSN (Electronic): 1875-6190
                Publication date (Print): December 2014
                Publication date (Electronic): December 2014
                Volume: 12
                Issue: 6
                Pages: 509-526
                Affiliations
                Department of Physiology, Medical Phaculty, Medical University, 1431 Sofia, Country Bulgaria
                Author notes
                [* ]Address correspondence to this author at the Department of Physiology, Medical Phaculty, Medical University, 1431 Sofia, Country Bulgaria; Tel: +35929172543; Mobile: +359887480853; Fax: +35929520345; E-mail: epopova@ 123456abv.bg
                Article
                Publisher ID: CN-12-509
                DOI: 10.2174/1570159X13999150122165018
                PMC ID: 4428025
                PubMed ID: 25977678
                SO-VID: 2c3ea74b-c891-40dd-b312-c980d7dfc133
                Copyright © © 2014 Bentham Science Publishers
                License:

                This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

                History
                Date received : 25 August 2014
                Date revision received : 19 December 2014
                Date accepted : 22 December 2014
                Categories
                Subject: Article

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: bipolar cells,electroretinogram,gaba,ganglion cells,glycine,on-off interactions,retina
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: bipolar cells, electroretinogram, gaba, ganglion cells, glycine, on-off interactions, retina

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