Journal
NEUROCHEMICAL RESEARCH
Volume 41, Issue 6, Pages 1229-1236Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-015-1792-x
Keywords
Retina; Glaucoma; Diabetes retinopathy; Energy metabolism; Lactate transport; Lactate receptor; Transmitter
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Funding
- University of Oslo
- Anders Jahre's Foundation for the Advancement of Science
- Norwegian Research Council (including Unikard, a joint Research Council-Health Authority Grant), Norway
- University of Copenhagen
- Velux Foundation
- Lundbeck Foundation, Denmark
- Lundbeck Foundation [R194-2015-948, R108-2012-10883] Funding Source: researchfish
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In retina, like in brain, lactate equilibrates across cell membranes via monocarboxylate transporters and in the extracellular space by diffusion, forming a basis for the action of lactate as a transmitter of metabolic signals. In the present paper, we argue that the lactate receptor GPR81, also known as HCAR1, may contribute importantly to the control of retinal cell functions in health and disease. GPR81, a G-protein coupled receptor, is known to downregulate cAMP both in adipose and nervous tissue. The receptor also acts through other down-stream mechanisms to control functions, such as excitability, metabolism and inflammation. Recent publications predict effects of the lactate receptor on neurodegeneration. Neurodegenerative diseases in retina, where the retinal ganglion cells die, notably glaucoma and diabetic retinopathy, may be linked to disturbed lactate homeostasis. Pilot studies reveal high GPR81 mRNA in retina and indicate GPR81 localization in Muller cells and retinal ganglion cells. Moreover, monocarboxylate transporters are expressed in retinal cells. We envision that lactate receptors and transporters could be useful future targets of novel therapeutic strategies to protect neurons and prevent or counteract glaucoma as well as other retinal diseases.
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