Spontaneous neuronal regeneration in the forebrain of the leopard gecko (Eublepharis macularius) following neurochemical lesioning. Issue 1 (30th August 2022)

• Record Type: Journal Article
• Authors: Austin, Laura E.; Graham, Chloe; Vickaryous, Matthew K.
• Other Names: Deans Michael R. guestEditor.; Williams Megan E. guestEditor.; Kale Shubham guestEditor.
• Is Part Of: Developmental dynamics. Volume 252:Issue 1(2023)
• Page Start: 186
• Page End: 207
• Publication Date: 2022-08-30
• Subjects: brain -- lizard -- medial cortex -- microglia -- neurogenesis -- regeneration -- reptile -- squamate; Morphogenesis -- Periodicals; Anatomy -- Periodicals; Anatomie -- Périodiques; Biologie du développement -- Périodiques; 571.833
• DOI: 10.1002/dvdy.525
• Languages: English
• ISSNs: 1058-8388

Abstract

Abstract: Background: Neurogenesis is the ability to generate new neurons from resident stem/progenitor populations. Although often understood as a homeostatic process, several species of teleost fish, salamanders, and lacertid lizards are also capable of reactive neurogenesis, spontaneously replacing lost or damaged neurons. Here, we demonstrate that reactive neurogenesis also occurs in a distantly related lizard species, Eublepharis macularius, the leopard gecko. Results: To initiate reactive neurogenesis, the antimetabolite 3‐acetylpyridine (3‐AP) was administered. Four days following 3‐AP administration there is a surge in neuronal cell death within a region of the forebrain known as the medial cortex (homolog of the mammalian hippocampal formation). Neuronal cell death is accompanied by a shift in resident microglial morphology and an increase neural stem/progenitor cell proliferation. By 30 days following 3‐AP administration, the medial cortex was entirely repopulated by NeuN+ neurons. At the same time, local microglia have reverted to a resting state and cell proliferation by neural stem/progenitors has returned to levels comparable with uninjured controls. Conclusions: Together, these data provide compelling evidence of reactive neurogenesis in leopard geckos, and indicate that the ability of lizards to spontaneously replace lost or damaged forebrain neurons is more taxonomically widespread and evolutionarily conserved than previously considered. Key Findings: Leopard geckos are capable of reactive neurogenesis. The antimetabolite 3‐acetylpyridine induces cell death of neurons within the medical cortex. Neuronal cell death is associated with a shift in local microglia morphology from resting to activated, and behavioural deficits. Within 30 days, the medial cortex is repopulated by neurons, microglia have returned to a resting state morphology, and behavioural deficits are resolved.