AI Article Synopsis
- - The study investigates the effect of the drug FK962 on the growth of nerve cells from the trigeminal ganglion, specifically looking at its ability to stimulate neurite elongation and regeneration after trigeminal nerve amputation.
- - Methods included culturing mixed trigeminal ganglion cells with FK962, using immunocytochemistry to observe neurite growth, and testing the release of specific factors like GDNF (glial cell line-derived neurotrophic factor) that are involved in nerve regeneration.
- - Results indicated that FK962 promotes neurite elongation by increasing GDNF production, suggesting that GDNF plays a role in the neurite regeneration process stimulated by FK962 in rat trigeminal neurons.
Article Abstract
Purpose: Amputation of the trigeminal nerve leads to decreased corneal sensitivity and dry eye. Our previous study showed that the drug FK962 (N-[1-acetylpiperidin-4-yl]-4-fluorobenzamide) induced neurite elongation from trigeminal ganglion (TG) cells and accelerated recovery of corneal sensitivity in a rabbit model of in situ keratomileusis (LASIK) surgery. However, the molecular pathways leading to FK962-induced neurite elongation and regeneration are not well defined. Thus, the purposes of the present experiments were to determine if FK962 induces elongation and regeneration of cultured rat TG cells and to investigate the mechanism of FK962-induced neurite elongation.
Methods: Mixed TG cells were cultured with or without FK962, and immunocytochemistry was used to detect stimulation of neurite elongation. Neurite regeneration was also tested in an in vitro model of neuronal ablation. ELISA was used to detect glial cell line-derived neurotrophic factor (GDNF) and somatostatin (SST) release, and mRNA expression was measured by qPCR. Antibody neutralization was used to determine the mechanism for FK962-induced neurite elongation/regeneration.
Results: FK962 enhanced elongation and regeneration of neurites in TG neurons. GDNF treatment-induced neurite elongation and GDNF antibody significantly inhibited neurite elongation induced by GDNF and FK962. Nerve growth factor (NGF) treatment also induced neurite elongation, which was inhibited by NGF antibody, but NGF antibody did not inhibit FK962-induced neurite elongation.
Conclusions: Our data suggested that FK962 stimulated induction of GDNF from TG cells. GDNF may be a part of the signaling pathway for FK962-induced neurite elongation/regeneration in rat TG neurons.
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| http://dx.doi.org/10.1167/iovs.11-8957 | DOI Listing |
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