Figure 7. C. elegans and mammalian neurons share degenerative mechanisms triggered by diverse pro-degenerative stimuli. The mechanisms associated to somatic and axonal degeneration of AVM-
mec-4d neurons were studied by pharmacological and genetic means. Worms were grown for 72 hours after hatching in food supplemented with EGTA (50 mM) or cyclosporin A (CsA, 50 mM). Both drugs delay degeneration of AVM somas (A) and axons (B) several fold (mean value for each category is shown; error bars [,1%] not included; N= 3 of 30 worms each per group; *p,0.01 by Student's t test compared with control for the SoW and AxW category). (C) Fluorescent micrograph of a beaded axon (AxB) and a vacuolated soma (SoV) of a
mec-4d-expressing AVM, contrasted with an AVM neuron treated with EGTA displaying a wild-type axon (AxW) and soma (SoW). Scale bar, 10 mm. (D) Touch neuron-specific expression of
nmat-2::gfp (Pmec-18nmat-2::gfp), which is restricted to the cytosol in all TRNs. Scale bar, 10 mm. Overexpression of NMAT-2::GFP in TRN protects to a large extent somas (E) and axons (F) from
mec-4d dependent degeneration at 72 hours post hatching (mean value for each category is shown; error bars [,0.1%] are not included; N= 3 of 30 worms each per group; *p,0.01 by Student's t test compared with control for the SoW and AxW category). (G) Anterior touch response of worms at 72 hours post hatching. The almost complete functional impairment triggered by
mec-4d is significantly rescued by NMAT-2::GFP overexpression (mean values are shown, error bars indicates SEM, N= 3 of 30 worms each per group; p,0.05 by Student's t test for touch sensitivity values).