September 1994
Volume 35, Issue 10
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Articles  |   September 1994
Glycine receptors in the retinas of normal and spastic mutant mice.
Author Affiliations
  • L H Pinto
    Department of Neurobiology and Physiology, Northwestern University, Evanston, IL 60208.
  • U Grünert
    Department of Neurobiology and Physiology, Northwestern University, Evanston, IL 60208.
  • K Studholme
    Department of Neurobiology and Physiology, Northwestern University, Evanston, IL 60208.
  • S Yazulla
    Department of Neurobiology and Physiology, Northwestern University, Evanston, IL 60208.
  • J Kirsch
    Department of Neurobiology and Physiology, Northwestern University, Evanston, IL 60208.
  • C M Becker
    Department of Neurobiology and Physiology, Northwestern University, Evanston, IL 60208.
Investigative Ophthalmology & Visual Science September 1994, Vol.35, 3633-3639. doi:
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    • Get Citation

      L H Pinto, U Grünert, K Studholme, S Yazulla, J Kirsch, C M Becker; Glycine receptors in the retinas of normal and spastic mutant mice.. Invest. Ophthalmol. Vis. Sci. 1994;35(10):3633-3639.

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

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Abstract

PURPOSE: Spastic mutant mice have abnormal gait and righting behavior, and the responses of their retinal ganglion cells have recently been shown to be abnormal. The former defects have been linked to a reduction of glycine-receptor density in the spinal cord of spastic mutants, but the cause of the retinal defects has not yet been determined. The authors thus tested for reduced glycine-receptor density in the mutant retina by comparing the levels of glycine receptors in the retinas of spastic mutant mice with those found in normal mice. METHODS: Indirect immunofluorescence histochemistry was employed, using monoclonal antibodies directed against the alpha- and beta-subunits of the receptor and against the 93-kd cytoplasmic receptor-associated protein, gephyrin. RESULTS: In normal mice, all glycine-receptor antibodies labeled two laminae of the inner plexiform layer (IPL): a broad band in the distal third of the IPL and a narrow band in the middle of the IPL. Lighter labeling was also seen in the outer plexiform layer with these antibodies. In spastic mutant mice, the glycine-receptor labeling of the IPL was reduced markedly. However, the overall structure of the spastic mutant retina was not disrupted because the distribution and intensity of both a presynaptic marker (synaptophysin) and a marker for the rod bipolar cell (protein kinase C) in the mutant retina were indistinguishable from those in normal retinas. CONCLUSIONS: The glycine-receptor distribution in normal mice was consistent with that previously reported for the rat and with the distribution of glycine responsiveness of dissociated rodent bipolar cells. The reduced levels of glycine receptors in spastic mice help explain the abnormal ganglion cell responses in the spastic mutant.

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