International Journal of Molecular Sciences · 8 authors, 5 centres
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This preclinical study used a guinea pig model of tear-deficient dry eye to show that topical cyclosporine A (CsA) acutely reduces the heightened cold-sensitivity of corneal nerve terminals. The results suggest a direct neural mechanism may contribute to CsA's clinical benefits in dry eye disease.
This preclinical study investigated the effect of cyclosporine A (CsA) on corneal cold thermoreceptor activity in a guinea pig model of tear-deficient dry eye (DE). Researchers recorded nerve terminal impulses (NTIs) from corneal cold receptors in vitro, both before and after CsA application. They also measured blinking frequency and tearing rate in awake animals. The central finding was that CsA significantly decreased the peak response to cold stimulation in cold thermoreceptors from tear-deficient animals, but did not affect spontaneous discharge rate or cooling threshold. CsA also appeared to reverse some changes in NTI shape induced by tear deficiency. In vivo, CsA increased both blinking and tearing in both control and tear-deficient animals. The study suggests that CsA has a direct, acute effect on hyperexcitable sensory nerve endings in DE, which may partly explain its clinical efficacy. Limitations include the use of an animal model with indirect human relevance, the need for further research to clarify the precise neural mechanisms, and the analysis of a limited number of tear-deficient nerve terminals for NTI shape.
