September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Impact of MCT4 deletion and MCT1 haploinsufficiency on the mouse retina
Author Affiliations & Notes
  • Neal S Peachey
    Cole Eye Institute/Cleveland VAMC, Cleveland Clinic Foundation, Cleveland, Ohio, United States
  • Carol Diallo
    Pathology, Anatomy, and Cell Biology, Thomas Jefferson University, Philadelphia, Pennsylvania, United States
  • Minzhong Yu
    Cole Eye Institute/Cleveland VAMC, Cleveland Clinic Foundation, Cleveland, Ohio, United States
  • Nancy J Philp
    Pathology, Anatomy, and Cell Biology, Thomas Jefferson University, Philadelphia, Pennsylvania, United States
  • Footnotes
    Commercial Relationships   Neal Peachey, None; Carol Diallo, None; Minzhong Yu, None; Nancy Philp, None
  • Footnotes
    Support  NIH Grant R01 EY012042; VA Grant I01 BX002340; Foundation Fighting Blindness; Research to Prevent Blindness
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 5771. doi:
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    • Get Citation

      Neal S Peachey, Carol Diallo, Minzhong Yu, Nancy J Philp; Impact of MCT4 deletion and MCT1 haploinsufficiency on the mouse retina. Invest. Ophthalmol. Vis. Sci. 2016;57(12):5771.

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

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Abstract

Purpose : In the vertebrate retina monocarboxylate transporters MCT1 and MCT4 are expressed in photoreceptor cells and Müller cells, respectively. The distribution of these transporters suggests that lactate shuttling between Müller cells and photoreceptor cells places a role in supporting retinal metabolism and photoreceptor cell function. To test this hypothesis we examined MCT4-/- and MCT1+/- mutant mice.

Methods : Visual function was evaluated by electroretinogram (ERG) and visual evoked potential (VEP) techniques. Retinal anatomy was evaluated by optical coherence tomography and immunohistochemistry. Gene expression was examined by quantitative PCR.

Results : All measures of visual function and retinal structure were normal in MCT1+/- mutant mice; MCT1-/- mice do not survive. In comparison, MCT4-/- mice survive and are indistinguishable from WT animals. ERG measures and retinal structure were comparable between MCT4-/- and WT littermates. This may reflect an upregulation of MCT5 in the MCT4-/- retina. VEPs were delayed in MCT4-/- mice, but an anatomical correlate was not observed in the inner retina.

Conclusions : The lack of an effect of MCT4 deletion on the outer retina may indicate that its role in metabolic support may be redundant with another retinal MCT or that the upregulation of MCT5 was an important compensatory response. Delayed VEPs in MCT4-/- mice may indicate an important role of MCT4 in support of inner retinal metabolism. A single allele of MCT1 appears to be sufficient to supports its potential role in the outer retina. To determine whether the lactate shuttle plays a role in supporting visual function will require the cell specific deletion of MCTs.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.

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