Establishing a Mouse Model of Chlorpromazine-Induced Corneal Trigeminal Denervation.

Purpose: This study aimed to establish a mouse model of chlorpromazine-induced corneal trigeminal denervation (CCTD).

Methods: Retrobulbar chlorpromazine injections were administered to 6- to 8-week-old C57BL/6j mice to induce corneal denervation. Additionally, apoptosis was assessed in isolated primary trigeminal ganglion cells after culturing in a conditioned medium containing chlorpromazine.

Trigeminal nerve-derived substance P regulates limbal stem cells by the PI3K-AKT pathway.

Trigeminal nerve-derived substance P (SP), a widespread neuropeptide, is known to maintain the corneal epithelial homeostasis and promote the closure of wound healing. Using comprehensive and assays and RNA-sequencing analysis, we aimed to unveil the positive effects of SP on the biological characteristics of limbal stem cells (LSCs) and the underlying mechanism. SP enhanced the proliferation and stemness of LSCs Correspondingly, it rescued corneal defects, corneal sensitivity, and the expression of LSC-positive markers in a neurotrophic keratopathy (NK) mouse model .