| First Author | Berkowitz BA | Year | 2017 |
| Journal | Neurobiol Aging | Volume | 49 |
| Pages | 198-203 | PubMed ID | 27823846 |
| Mgi Jnum | J:276540 | Mgi Id | MGI:6315007 |
| Doi | 10.1016/j.neurobiolaging.2016.09.009 | Citation | Berkowitz BA, et al. (2017) Genetically heterogeneous mice show age-related vision deficits not related to increased rod cell L-type calcium channel function in vivo. Neurobiol Aging 49:198-203 |
| abstractText | Visual performance declines over time in humans and 2-18 months outbred Long-Evans (LE) rats; vision is maintained in inbred 2-18 months C57BL/6 (B6) mice. Increased rod L-type calcium channel (LTCC) function predicts visual decline in LE rats but does not occur in B6 mice. Genetic diversity may contribute to rod LTCC function escalation time. To test this hypothesis, 4 and 18 months genetically heterogeneous UM-HET3 mice were studied. Rod LTCC function (manganese-enhanced magnetic resonance imaging [MRI]) and ocular anatomy (MRI, optical coherence tomography) were measured in vivo. Light-evoked subretinal space and choroid thickness changes were measured (diffusion-weighted MRI). Visual performance declined over time in the absence of (1) increased rod LTCC function; (2) changes in light-dependent expansion of the subretinal space and choroidal thickness; and (3) retinal thinning. Aging changed anterior and vitreous chambers' axial length and decreased light-stimulated choroidal expansion. Species differences appear to contribute to the LTCC function differences. Aging-related declines in vision in the UM-HET3 mice deserve more attention than they have received so far. |
