June 2023
Volume 64, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2023
Neuropeptide Y overexpression in the presence of P23H rhodopsin mutation
Author Affiliations & Notes
  • Jean Sun
    Neurobiology, The University of Alabama at Birmingham Heersink School of Medicine, Birmingham, Alabama, United States
  • Mary Anne Garner
    Neurobiology, The University of Alabama at Birmingham Heersink School of Medicine, Birmingham, Alabama, United States
  • Lynn Dobrunz
    Neurobiology, The University of Alabama at Birmingham Heersink School of Medicine, Birmingham, Alabama, United States
  • Aundrea Bartley
    Neurobiology, The University of Alabama at Birmingham Heersink School of Medicine, Birmingham, Alabama, United States
  • Alecia K Gross
    Neurobiology, The University of Alabama at Birmingham Heersink School of Medicine, Birmingham, Alabama, United States
  • Footnotes
    Commercial Relationships   Jean Sun None; Mary Anne Garner None; Lynn Dobrunz None; Aundrea Bartley None; Alecia Gross None
  • Footnotes
    Support  NIH Grant MH108342, NIH Grant EY030096
Investigative Ophthalmology & Visual Science June 2023, Vol.64, 4864. doi:
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    • Get Citation

      Jean Sun, Mary Anne Garner, Lynn Dobrunz, Aundrea Bartley, Alecia K Gross; Neuropeptide Y overexpression in the presence of P23H rhodopsin mutation. Invest. Ophthalmol. Vis. Sci. 2023;64(8):4864.

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

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Abstract

Purpose : The P23H opsin mutation (RhoP23H) is the most common cause of rhodopsin-mediated autosomal dominant retinitis pigmentosa (adRP), a degenerative blinding condition. Neuropeptide Y (NPY) is a peptide neurotransmitter with multiple neuroprotective functions observed in central nervous system. Both NPY and its receptors are found in retinal tissue, yet the role of NPY and its receptors in retina remain unknown. We hypothesize that due to its neuroprotective effects, the overexpression of NPY may slow photoreceptor degeneration in RP.

Methods : We obtained homozygous NPY over-expressing (NpyOE) mice as well as both RhoP23H/+ and RhoP23H/P23H mice. At 6 weeks of age, we analyzed the retinal function of RhoP23H/P23H and NpyOE mice using electroretinography (ERG). We are continuing to analyze the retinal function of RhoP23H/P23H, NpyOE, RhoP23H/P23H NpyOE, and RhoP23H/+ NpyOE mice at 3, 6, and 15 weeks of age. At the same time points, we are using immunohistochemistry to validate the expression of NPY and its receptors in the retina and are staining for apoptotic and autophagy markers to determine whether overexpression of NPY attenuates the effect of the RhoP23.

Results : While the RhoP23H/P23H mice have significant reductions both in a- and b-wave amplitudes in scotopic and photopic conditions at 6 weeks, NpyOE alone has no effect on wave amplitudes in scotopic conditions compared with wild type animals. Interestingly, under photopic conditions, NPYOE alone exhibited a trend towards a reduction in the photopic a-wave amplitude.

Conclusions : We have found that NPY overexpression alone does not appreciably affect retinal function. We are continuing to determine the level of NPY overexpression in the retina as well as the effect of NPY overexpression on NPY receptor levels, and we are gathering data to determine whether we see a delay in degeneration and retinal function in the RhoP23H/+ NPYOE and RhoP23H/P23H NPYOE mice.

This abstract was presented at the 2023 ARVO Annual Meeting, held in New Orleans, LA, April 23-27, 2023.

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