| First Author | Arnold E | Year | 2020 |
| Journal | Neurobiol Aging | Volume | 85 |
| Pages | 38-48 | PubMed ID | 31698287 |
| Mgi Jnum | J:285568 | Mgi Id | MGI:6391764 |
| Doi | 10.1016/j.neurobiolaging.2019.10.002 | Citation | Arnold E, et al. (2020) Prolactin mitigates deficiencies of retinal function associated with aging. Neurobiol Aging 85:38-48 |
| abstractText | Aging causes the progressive degeneration of retinal cells leading to the eventual loss of vision. The hormone prolactin (PRL) is a neurotrophic factor able to compensate for photoreceptor cell death and electroretinogram deficits induced by light retinal damage. Here, we used adult 4-month old and aged 20-month old pigmented mice, null or not for the PRL receptor to explore whether PRL provides trophic support against age-related retinal dysfunction. Retinal functionality, apoptosis, glia activation, and neurotrophin expression were assessed by electroretinogram, TUNEL, glial fibrillary acidic protein and ionized calcium binding adaptor molecule 1 immunohistochemistry, and real-time PCR, respectively. Lack of PRL signaling in aged mice, but not in adult mice, correlated with photosensitive retinal dysfunction, increased photoreceptor apoptosis, differential expression of proapoptotic mediators, and microglia activation. We conclude that PRL is required for maintaining retinal functionality in both female and male mice during aging and has potential therapeutic value against age-related retinal disorders. |
