Abstract
We previously reported that in the superior cervical ganglion (SCG) of dystrophic mdx mice, which lack full-length dystrophin, there is a loss of neurons projecting to SCG muscular targets, like the iris. Nonetheless, surviving neurons, innervating either iris or submandibular gland (SuGl), a SCG non-muscular target, underwent reduced axon defasciculation and terminal branching. Here we report that, during early post-natal development, levels of pro-apoptotic proNGF in mdx mouse iris, but not in the SuGl, are higher than in the wild-type. This increase, along with reduced levels of NGF receptors (TrkA and p75NTR) in SCG, may be partly responsible for the observed loss of neurons projecting to the iris. These alterations, combined with a reduction in polysialylated-NCAM and neurofilament protein levels in SCG, may also account for reduced axon defasciculation and terminal branching in mdx mouse SCG targets.