Journal
JOURNAL OF NEUROSCIENCE
Volume 34, Issue 5, Pages 1868-1878Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.2452-13.2014
Keywords
gliosis; prolactin; retinal degeneration; trophic factor
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Funding
- Universidad Nacional Autonoma de Mexico (UNAM)
- National Council of Science and Technology of Mexico (CONACYT) [176393]
- CONACYT [99210]
- UNAM posgrado program
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Retinal degeneration is characterized by the progressive destruction of retinal cells, causing the deterioration and eventual loss of vision. We explored whether the hormone prolactin provides trophic support to retinal cells, thus protecting the retina from degenerative pressure. Inducing hyperprolactinemia limited photoreceptor apoptosis, gliosis, and changes in neurotrophin expression, and it preserved the photoresponse in the phototoxicity model of retinal degeneration, in which continuous exposure of rats to bright light leads to retinal cell death and retinal dysfunction. In this model, the expression levels of prolactin receptors in the retina were upregulated. Moreover, retinas from prolactin receptor-deficient mice exhibited photoresponsive dysfunction and gliosis that correlated with decreased levels of retinal bFGF, GDNF, and BDNF. Collectively, these data unveiled prolactin as a retinal trophic factor that may regulate glial-neuronal cell interactions and is a potential therapeutic molecule against retinal degeneration.
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