Retinal insulin receptors: localization using a polyclonal anti-insulin receptor antibody

Rodrigues, Merlyn; Waldbillig, Robert J.; Rajagopalan, Sumati; Hackett, Jeremiah D.; LeRoith, Derek; Chader, Gerald J.

doi:10.1016/0006-8993(88)91639-3

Cited by 45 publications

(36 citation statements)

References 15 publications

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“…org as supplemental material). The presence of IGF-1 receptors at such an early age is in line with previous papers showing that IGF-1 receptors are present very early in the retina (Rodrigues et al, 1988;Waldbillig et al, 1988;Lee et al, 1992;Lofqvist et al, 2009) and, in particular, in the rat retina, already at P0 (Lee et al, 1992). At P0, they are expressed in the RGC layer and in the optic nerve fiber layer (Lee et al, 1992).…”

Section: Igf-1 Mediates the Effects Of Ee On Retinal Acuity Developmentsupporting

confidence: 89%

Setting the Pace for Retinal Development: Environmental Enrichment Acts Through Insulin-Like Growth Factor 1 and Brain-Derived Neurotrophic Factor

Landi

Ciucci²,

Maffei³

et al. 2009

J. Neurosci.

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Environmental enrichment strongly affects visual system maturation both at retinal and cortical levels. Which molecular pathways are activated by an enriched environment (EE) to regulate visual system development has not been clarified. Here, we show that early [postnatal day 1 (P1) to P7] insulin-like growth factor 1 (IGF-1) injections in the eyes of non-EE rat pups mimic EE effects both in increasing BDNF levels in the retinal ganglion cell layer at P10 and in determining a more adult-like retinal acuity, assessed with pattern electroretinogram at P25. Blocking IGF-1 action in EE animals during the same early postnatal time window by injecting the IGF-1 receptor antagonist JB1 prevents EE effects both on BDNF expression and on retinal acuity maturation. Reducing BDNF expression in the retina of IGF-1-treated rats prevents IGF-1 effects on retinal acuity development. Finally, we show that tyrosine hydroxylase (TH) expression is increased in the retina of P10 EE and IGF-1-treated rats and that blocking TH expression in EE animals prevents EE from affecting retinal acuity development. Thus, early levels of IGF-1 play a key role in mediating EE effects on retinal development through an action that requires BDNF and involves dopaminergic amacrine cell network.

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Section: Igf-1 Mediates the Effects Of Ee On Retinal Acuity Developmentsupporting

confidence: 89%

Setting the Pace for Retinal Development: Environmental Enrichment Acts Through Insulin-Like Growth Factor 1 and Brain-Derived Neurotrophic Factor

Landi

Ciucci²,

Maffei³

et al. 2009

J. Neurosci.

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“…Many reports show that insulin and insulin-like growth factors (IGFs) play an important role in retinal growth and survival (Hernandez-Sanchez et al, 1995;Frade et al, 1996;Alarcon et al, 1998;Barber et al, 2001). Insulin and IGF1 receptors are found in the retina of several species, including Drosophila, chick, mice, and humans (Rodrigues et al, 1988;Bassnett and Beebe, 1990;Bronson et al, 2003). IGF1 stimulates the generation of differentiated neurons in neuroepithelial cell cultures from embryonic chick neural retina (Alarcon et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Insulin Receptor Substrate 2 Is Essential for Maturation and Survival of Photoreceptor Cells

Schubert

Peachey

et al. 2005

J. Neurosci.

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Insulin receptor substrates (Irs-proteins) integrate signals from the insulin and insulin-like growth factor-1 (IGF1) receptors with other processes to control cellular growth, function, and survival. Here, we show that Irs2 promoted the maturation and survival of photoreceptors in the murine retina immediately after birth. Irs2 was mainly localized to the outer plexiform layer as well as to photoreceptor inner segments. It was also seen in ganglion cells and inner plexiform layer but in smaller amounts. Compared with control littermates, Irs2 knock-out mice lose ϳ10% of their photoreceptors 1 week after birth and up to 50% by 2 weeks of age as a result of increased apoptosis. The surviving photoreceptor cells developed short organized segments, which displayed proportionally diminished but otherwise normal electrical function. However, IGF1-stimulated Akt phosphorylation was barely detected, and cleaved/activated caspase-3 was significantly elevated in isolated retinas of Irs2 Ϫ/Ϫ mice. When diabetes was prevented, which allowed the Irs2 Ϫ/Ϫ mice to survive for 2 years, most photoreceptor cells were lost by 16 months of age. Because apoptosis is the final common pathway in photoreceptor degeneration, pharmacological strategies that increase Irs2 expression or function in photoreceptor cells could be a general treatment for blinding diseases such as retinitis pigmentosa.

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“…InsRs are located on both the inner and outer segments of vertebrate photoreceptors [8] and insulin has been shown to produce a dose-dependent decrease in the a-and b-waves of the electroretinogram (ERG) [9]. The ERG b-wave reflects the activity of inputs from photoreceptors onto ON depolarizing bipolar cells [10].…”

Section: Introductionmentioning

confidence: 99%

Insulin inhibits voltage-dependent calcium influx into rod photoreceptors

2001

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Insulin inhibits the ERG b-wave and modulates L-type calcium currents (I Ca ) in various preparations. We therefore examined insulin's effects on I Ca and depolarization-evoked [Ca 2+ ] i increases in rod photoreceptors. Insulin inhibited I Ca and caused a dose-dependent reduction in the depolarizationevoked Ca 2+ influx with an EC 50 of 2.1 nM. Tyrosine kinase inhibitors, lavendustin A (100 nM) and genistein (10 μM), prevented insulin from reducing the depolarization-evoked Ca 2+ increase in rods. Their less active analogues, lavendustin B and daidzein, had similar effects. An insulin receptorspecific tyrosine kinase inhibitor, HNMPA-(AM) 3 (50 μM), prevented insulin (30 nM) from reducing the depolarization-evoked Ca 2+ increase in rods. The results suggest that insulin inhibits Ca 2+ influx through voltage-dependent I Ca in rod photoreceptors via tyrosine kinase activity.

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Retinal insulin receptors: localization using a polyclonal anti-insulin receptor antibody

Cited by 45 publications

References 15 publications

Setting the Pace for Retinal Development: Environmental Enrichment Acts Through Insulin-Like Growth Factor 1 and Brain-Derived Neurotrophic Factor

Setting the Pace for Retinal Development: Environmental Enrichment Acts Through Insulin-Like Growth Factor 1 and Brain-Derived Neurotrophic Factor

Insulin Receptor Substrate 2 Is Essential for Maturation and Survival of Photoreceptor Cells

Insulin inhibits voltage-dependent calcium influx into rod photoreceptors

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