4.3 Article

Expression of BDNF and NT-3 During the Ontogeny and Regeneration of the Lacertidian (Gallotia galloti) Visual System

Journal

DEVELOPMENTAL NEUROBIOLOGY
Volume 71, Issue 10, Pages 836-853

Publisher

WILEY
DOI: 10.1002/dneu.20939

Keywords

optic pathway; regeneration; development; reptiles; trophic support

Funding

  1. Spanish Ministry of Education [BFU2007-67139]
  2. Regional Canary Island Government (ACIISI) [SolSubC200801000281, ULPAPD-08/01-4]
  3. University of Las Palmas de Gran Canaria

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Retinal ganglion cell (RGC) axons regrow spontaneously after optic nerve (ON) transection in G. galloti. Because brain-derived neurotrophic factor (BDNF) is considered the major neurotrophin participating in vertebrate visual system development and promotes RGC survival, we investigated its distribution using dual-labeling immunohistochemistry for neuronal and glial markers. We examined the developing and regenerating lizard visual system at 1, 3, 6, 9, and 12 months postlesion to comparatively evaluate BDNF expression patterns. BDNF was detected from midembryonic stages (E35) in both retinal plexiform layers, and in radial glial processes in the tectum. Moreover, RGC axon staining was detected at late prenatal stages (E39), showing a transient punctate staining which progressed in a temporo-spatial pattern that was similar to myelination. Strong expression in RGC axons was maintained in adults. However, transient downregulation of BDNF staining occurred on the experimental side one month after ON transection followed by a gradual recovery with extensive punctate/swelling distribution and persistent upregulation at 12 months. Conversely, quantitative PCR analysis for 1 and 12 months regenerate lizards showed downregulation of the ratio of BDNF mRNA expression at 12 months and nonsignificant changes of NT-3 transcripts. In summary, we demonstrate that BDNF and NT-3 are abundantly expressed during lizard visual system ontogeny and regeneration suggesting their participation in the development, maintenance and plasticity of the system. (C) 2011 Wiley Periodicals, Inc. Develop Neurobiol 71: 836-853, 2011

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