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P. de la Villa, L. Rodriguez de la Rosa, L. Fernandez Sanchez, S. Murillo Cuesta, I. Varela-Nieto, N. Cuenca; Functional and Structural Retinal Modifications in the Igf1-/- Null Mouse. Invest. Ophthalmol. Vis. Sci. 2010;51(13):2488.
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© ARVO (1962-2015); The Authors (2016-present)
It has been reported that mutations in the gene encoding human insulin-like growth factor-I (IGF-I) cause syndromic sensory dysfunction. To study the precise role of IGF-I in retinal physiology and to hypothesize the possible morphological and electrophysiological changes that may occur in the retina, we have focused on a mouse model of IGF-I deficiency (Igf1-/- homozygous null mice) in comparison with Igf1-/+ heterozygous and wild type (wt) animals.
We have analyzed the retinal function by means of electroretinographic (ERG) responses and the retinal morphology by the use of immunocytochemical labeling on retinal preparations.
We show that homozygous Igf1-/- mice, by postnatal age of 360 days (P360) have an almost flat scotopic ERG response; photopic ERG response is detectable, but of very small amplitude. At the same age, heterozygous Igf1-/+ mice still show both scotopic and photopic ERG responses, but a significant decrease in the ERG wave amplitudes is observed, when compared with wt mice. Immunocytochemical analysis show that homozygous Igf-1-/- mice at P360 suffer important structural modifications in the first synapse of the retinal pathway, that affect mainly to the postsynaptic processes from horizontal and bipolar cells. A decrease in bassoon and synaptophysin staining in both rod and cone synaptic terminals points to reduced photoreceptor output to the inner retina. Retinal morphology of the heterozygous Igf1-/+ mice just show small alterations in the horizontal and bipolar cells processes, when comparing with wt mice. Levels of IGF-I levels. A correlation between the serological levels of IGF-I and phenotype manifestations is observed in the heterozygous Igf1-/+ mice.
The present results support the use of the Igf-1-/- mouse as a new model for the study of human syndromic blindness.
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