Impact of MCT1 Haploinsufficiency on the Mouse Retina.
- Peachey NS Louis Stokes Cleveland VA Medical Center, Cleveland, OH, USA. neal.peachey@va.gov.
- Yu M Cole Eye Institute, Cleveland Clinic, Cleveland, OH, USA.
- Han JYS Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA, USA.
- Lengacher S Brain Mind Institute, Ecole Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland.
- Magistretti PJ Brain Mind Institute, Ecole Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland.
- Pellerin L Department of Physiology, University of Lausanne, Lausanne, Switzerland.
- Philp NJ Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA, USA.
- 2018-05-04
Published in:
- Advances in experimental medicine and biology. - 2018
Electroretinogram
Lactate
MCT1
Retina
Transgenic mice
Animals
Electroretinography
Energy Metabolism
Evoked Potentials, Visual
Heterozygote
Lactates
Mice
Mice, Inbred C57BL
Mice, Transgenic
Monocarboxylic Acid Transporters
Motor Neurons
Oligodendroglia
Photoreceptor Cells, Vertebrate
Retina
Retinal Bipolar Cells
Symporters
English
The monocarboxylate transporter 1 (MCT1) is highly expressed in the outer retina, suggesting that it plays a critical role in photoreceptors. We examined MCT1 +/- heterozygotes, which express half of the normal complement of MCT1. The MCT1 +/- retina developed normally and retained normal function, indicating that MCT1 is expressed at sufficient levels to support outer retinal metabolism.
- Language
-
- English
- Open access status
- green
- Identifiers
-
- DOI 10.1007/978-3-319-75402-4_46
- PMID 29721966
- Persistent URL
- https://sonar.ch/global/documents/278052
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