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In the present study, we investigated the potential changes in the corneal nerve terminals in non–insulin-dependent diabetes mellitus of moderate duration. The dissected corneas were subjected to a protocol of ultracentrifugation to obtain synaptosomes of sensory nerve terminals. Within these nerve varicosities, 2 major mechanisms were examined, viz., alterations of the mechanosensitive channel pannexin1 and ATP release on stimulation of these terminals. We hypothesized that altered cellular location and function of the pannexin channel may contribute to altered mechanosensitivity of the cornea, which in turn may affect wound healing and primary visual function of the cornea. The chief rationale for focusing on examining the pannexin channel is due to its role in mechanosensitivity, as well as its glycosylation property. Pannexin1 remains unchanged between diabetic subjects in comparison to nondiabetic controls. However, lectin immunoassay showed that pannexin1 is significantly more glycosylated in diabetic corneal synaptosomes. Membrane biotinylation assay showed that membrane localization of pannexin1 is significantly enhanced in diabetic samples. Furthermore, S-nitrosylation of the glyco-pannexin1 is significantly decreased in comparison to pannexin1 obtained from corneal varicosities of normoglycemic subjects. The diabetic corneal synaptosomes show enhanced ATP release after potassium chloride stimulation, when compared to controls. Furthermore, we have shown that S-nitrosylation of pannexin1 actually diminishes the ability of pannexin1 to release ATP. Thus, much like the peripheral nerves, the corneal nerves also show increased hypersensitivity in diabetes of chronic duration. All of these pathological changes may cumulatively alter corneal function in diabetes.

Increased membrane localization of pannexin1 in human corneal synaptosomes causes enhanced stimulated ATP release in chronic diabetes mellitus