Article

Impact of age and retinal degeneration on the light input to circadian brain structures.

University of Oxford, Circadian and Visual Neuroscience Group, Nuffield Laboratory of Ophthalmology, Level 5 and 6, West Wing, The John Radcliffe Hospital, Headley Way, Headington, Oxford OX3 9DU, UK.
Neurobiology of aging (impact factor: 5.94). 02/2012; 33(2):383-92. DOI:10.1016/j.neurobiolaging.2010.03.006 pp.383-92
Source: PubMed

ABSTRACT Aging causes anatomical and functional changes in visual and circadian systems. In wild type mice rods, cones, and photosensitive retinal ganglion cells (pRGCs) decline with age. In rd/rd cl mice, the early loss of rods and cones is followed by protracted transneuronal loss of inner retinal neurons as well as the pRGCs. Here we use Fos induction to study the light input pathway to the suprachiasmatic nuclei (SCN), the intergeniculate leaflets (IGL) and ventral lateral geniculate nuclei (vLGN) of old (∼700 days) and young (∼150 days) wild type and rd/rd cl mice. Cholera toxin tracing was used in parallel to study the anatomy of this pathway. We find that aging rather than retinal degeneration is a more important factor in reducing light input to the SCN, causing both a reduction in Fos expression and retinal afferents. Furthermore, we show light-induced Fos within the vLGN and IGL is predominantly subserved by rods and cones, and once again aging reduces the amplitude of this response.

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Keywords

Aging causes anatomical
 
anatomy
 
Cholera toxin tracing
 
circadian systems
 
inner retinal neurons
 
light input
 
light input pathway
 
light-induced Fos
 
pathway
 
photosensitive retinal ganglion cells
 
pRGCs
 
protracted transneuronal loss
 
rd/rd cl mice
 
retinal afferents
 
retinal degeneration
 
suprachiasmatic nuclei
 
ventral lateral geniculate nuclei
 
visual
 
vLGN
 
wild type mice rods
 

Daniela Lupi