Abstract
Purpose::
Past research has demonstrated changes in choroidal thickness, permeability, and blood flow during the compensation for myopic and hyperopic defocus. The current investigation suggests that the choroidal synthesis of the neuropeptides somatostatin and galanin may participate in these choroidal responses.
Methods::
Myopia was induced in White leghorn chicks by form deprivation for 10 days, followed by four days of unrestricted vision (recovery). Suprachoridal fluid was isolated from the posterior poles of enucleated treated and control eyes, tissue punches of posterior ocular tissues were obtained and immediately fixed in 4% paraformaldehyde, and choroids were isolated from treated and control eyes for total protein extraction. Dot blot analyses, immunohistochemistry and confocal microscopy were employed using commercially available anti-galanin and anti-somatostatin antibodies to determine the distribution and abundance of galanin and somatostatin in choroids and suprachoroidal fluid of recovering and control chick eyes. Comparisons between control and recovering eyes were made using paired t-tests.
Results::
Both galanin and somatostatin were found to be expressed in the stroma of the chick choroid and in association with blood vessels and neurons. Results from dot blot analyses indicated that galanin was down-regulated in recovering eyes over controls (- 50%, p<0.05, paired t-test, n = 3), while somatostatin was up-regulated (+ 75%, p<0.05, paired t-test, n = 3) (P<0.05). Somatostatin and galanin were also present in suprachoroidal fliud, suggesting choroidal release of these neuropeptides into choroidal vascular and/or lymphatic circulation.
Conclusions::
These data demonstrate changes in choroidal levels of galanin and somatostatin in response to myopic defocus at the molecular level, and suggest the involvement of choroidal neurons in ocular growth regulation.
Keywords: neuropeptides • choroid • myopia