The Neurogenic Effect of Injury and Regeneration in Ctenophores


Meeting Abstract

P2.29  Tuesday, Jan. 5  The Neurogenic Effect of Injury and Regeneration in Ctenophores ANDRILENAS, KK*; MOROZ, L; University of Washington, Seattle; Whitney Laboratory for Marine Biosciences, University of Florida, St. Augustine andrik@u.washington.edu

Studying how nervous systems evolved requires a broad investigation of many phyla. Ctenophores, one of the most basal organisms (Dunn, 2008), are an under researched group of organisms. The signaling molecules used by their neurons have yet to be documented, and few immunohistochemistry (IHC) experiments have been done. In the ctenophores Bolinopsis infundibulum and Pleurobrachia bachei, anti-FMRFamide IHC labels injury induced neurogenesis. Ctenophores were collected at Friday Harbor Labs, Friday Harbor, WA and kept in sea tables at local sea temperature. Ctenophores were dissected and the tissue was allowed to regenerate with culture times from first incision to fixation. B. infundibulum and P. bachei tissue was cultured for 0–3, 6, 24, and 72 hours with longer cultures for B. infundibulum. Tissue was then fixed and stained using anti-FMRFamide IHC protocols developed for the ctenophores. Neuron density and nerve net organization increased with the length of culture time. Preliminary data in P. bachei suggests they have a slower regeneration time. B. infundibulum has a amazing regenerative capacity and regenerates a robust neural network in 72 to 96 hours. An assessment of B. infundibulum apical organ regeneration was done and it takes only four days to regrow the statocyst, but more time is required for regeneration of the aboral canals. The labeling of a FMRFamide-like compound in post-injury neurogenesis suggests it may be a signaling molecule involved in regeneration. Moroz (in press) suggests that recruitment of damage related secretory pathways may have been an avenue for the evolution of neurons. Further research may reveal whether exogenous FMRFamide-like compound can induce neurogenesis.

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