Aim 

Somatostatin (SRIF) is a retinal peptide which plays important antiangiogenic roles. In a mouse model of oxygen induced retinopathy (OIR), the contribution of the SRIF receptor sst₂ to SRIF antiangiogenic action was examined. In addition, expression and localization of sst₂ was determined in the hypoxic retina. Moreover, retinal function was studied with electroretinography (ERG) in order to determine whether dysfunctional ERG may be influenced by selective activation or blockade of sst₂.

Methods 

OIR was induced in mouse retinas according to previous studies (Dal Monte et al.,IOVS, 48, 2007). Animals were treated with the sst₂ agonist octreotide (20 mg/kg/dose) or the sst₂ antagonist CYN (500 mg/kg/dose). Angiogenesis was evaluated in fluorescein-perfused retinas.Retinal localization of sst₂ was assessed by immunohistochemistry. ERG responses to full field stimuli were recorded from dark-adapted mice.

Results 

OIR-induced neovascularization was reduced by octreotide, whereas it was increased by sst₂ blockade with CYN. In OIR mice, retinal expression of sst₂ decreased in the neuroretina, whereas drastically increased at the level of growing vessels. In OIR mice, the amplitude of a- and b-waves and oscillatory potentials was smaller than in normoxic mice.Octreotide treatment significantly improved dysfunctional ERG that, in contrast, was not influenced by CYN.

Conclusion 

Our results demonstrate that hypoxia alters retinal vasculature and function. The finding that sst₂ activation reduces neovascularization and ameliorates retinal dysfunction further supports the possibility of the use of sst₂-selective ligands in the treatment of retinopathy.