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Age-related functional and structural retinal modifications in the Igf1-/- null mouse.

L Rodriguez-de la Rosa¹, L Fernandez-Sanchez, F Germain

¹Instituto de Investigaciones Biomédicas Alberto Sols, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, CIBERER Unit 761, ISCiii, IdiPAZ, Arturo Duperier 4, 28029 Madrid, Spain.

Neurobiology of Disease

|March 10, 2012

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Insulin-like growth factor-I (IGF-I) deficiency in mice leads to age-related vision loss and congenital deafness. This study highlights the Igf1(-/-) mouse as a model for human syndromic deaf-blindness.

Area of Science:

Neuroscience
Genetics
Ophthalmology

Background:

Mutations in the human insulin-like growth factor-I (IGF-I) gene are linked to syndromic neurosensorial deafness.
The role of IGF-I in retinal physiology requires further investigation.

Purpose of the Study:

To investigate the impact of IGF-I deficiency on retinal morphology and electrophysiology in mice.
To compare the aging effects on the retina of Igf1(-/-), Igf1(+/-), and Igf1(+/+) mice.

Main Methods:

Assessed serological IGF-I levels, glycemia, and body weight in mice up to 360 days of age.
Evaluated hearing using auditory brainstem responses (ABR).
Analyzed retinal function via electroretinography (ERG) and retinal structure through immunohistochemistry.

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Main Results:

IGF-I levels decrease with age in mice.
Igf1(-/-) mice exhibited severely impaired scotopic and photopic ERG responses and significant retinal structural changes, particularly in the synaptic pathways.
Igf1(+/-) mice showed reduced ERG amplitudes and minor retinal alterations compared to controls.

Conclusions:

IGF-I deficit in mice results in age-related visual impairment alongside congenital deafness.
The Igf1(-/-) mouse serves as a valuable model for studying human syndromic deaf-blindness.