Abstract

Neurogenesis is the ability to generate new neurons from resident progenitor populations. Although best understood as a normal physiological process, in several species of teleost fish and salamanders neurogenesis is also capable of replacing neurons lost or damaged due to injury – so called reactive neurogenesis. While reactive neurogenesis does not appear to resolve brain injuries in mammals, for reptiles less is known. Here, we investigated reactive neurogenesis in the lizard Eublepharis macularius, the leopard gecko. To initiate reactive neurogenesis, we administered geckos with a single dose of the neurotoxin 3‐acetylpyridine (3AP). Using the cell death markers Fluoro‐Jade and the TUNEL assay, we determined that neuronal loss occurs within 4 days following 3AP administration. Cell death is largely restricted to the medial and dorsomedial cortices, areas of the forebrain widely accepted to be the reptilian homologs of the mammalian hippocampus and neocortex, respectively. As evidenced by a decrease in the number of cells expressing the mature neuronal marker NeuN, cell death within these regions appears to selectively target neurons. Remarkably, by 30 days following 3AP administration the medial and dorsomedial cortices appear to be structurally restored with a pattern of NeuN expression that closely resembles the uninjured brain. These data provide the first evidence that the leopard gecko is capable of reactive neurogenesis, a phenomenon otherwise rare among amniotes (reptiles and mammals).Support or Funding InformationNatural Sciences and Engineering Research Council (NSERC), Discovery Grant 400358)

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call