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Lactate transport and receptor actions: Potential roles in inner retinal function and disease
Purpose In the brain and in adipose tissue activation of the lactate receptor GPR81 is known to promote downregulation of cAMP. Lactate is hereby involved in excitability, metabolism and inflammation. Neurodegenerative diseases in retina may in a similar manner be linked to disturbed lactate homeost...
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Published in: | Acta ophthalmologica (Oxford, England) England), 2015-10, Vol.93 (S255), p.n/a |
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Main Authors: | , , , , , , , , , , |
Format: | Article |
Language: | English |
Online Access: | Get full text |
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Summary: | Purpose
In the brain and in adipose tissue activation of the lactate receptor GPR81 is known to promote downregulation of cAMP. Lactate is hereby involved in excitability, metabolism and inflammation. Neurodegenerative diseases in retina may in a similar manner be linked to disturbed lactate homeostasis.
Methods
qPCR was performed on retina and brain extracts to investigate whether the lactate receptor GPR81 is expressed in the retina. Immunocytochemistry was performed on primary cell cultures of Müller cells (MC) and retinal ganglion cells (RGC) from mice to evaluate the presence of lactate receptors in neuronal and glial cells in the retina. Lactate assays were made to show the changes in lactate concentrations during different conditions of stress.
Results
GPR81 mRNA was twice as high in retina as in hippocampus or cerebral cortex. Immunocytochemistry indicated lactate receptors in both RGC and MC. Lactate assays showed a decreased release of lactate from MC upon energy restriction. Interestingly, the combination of inhibited mitochondrial function and energy restriction significantly increased the amount of released lactate.
Conclusions
The presence of lactate receptors in the retina as well as the changed levels of lactate in response to stress support the suggestion that lactate could be of great importance in retinal homeostasis and as such in the pathogenesis of inner retinal diseases. |
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ISSN: | 1755-375X 1755-3768 |
DOI: | 10.1111/j.1755-3768.2015.0601 |