Enriched environment during adolescence changes brain-derived neurotrophic factor and TrkB levels in the rat visual system but does not offer neuroprotection to retinal ganglion cells following axotomy

Tamara B. Franklin, Jeremy A. Murphy, Tanya L. Myers, David B. Clarke, R. William Currie

Research output: Contribution to journalArticlepeer-review

26 Citations (Scopus)

Abstract

The purpose of the present experiment was to characterize changes in TrkB signaling in the rat visual system resulting from exposure to enriched environment. Female Sprague-Dawley rats were placed in enriched or impoverished conditions for 1, 7 or 28 days. Levels of BDNF protein and its predominant receptor TrkB were examined in the retina, superior colliculus and visual cortex. In the retina, 1 day of enrichment increased full-length TrkB and after 28 days increased BDNF. In the superior colliculus, enrichment for 7 days reduced full-length TrkB and after 28 days increased BDNF and full-length TrkB. One day of enrichment significantly increased BDNF, reduced full-length TrkB and increased truncated TrkB in the visual cortex. Consequently, we further investigated whether exposure to enriched environment and the subsequent changes in BDNF and TrkB translates into a neuroprotective effect on retinal ganglion cells (RGCs) following transection of the optic nerve. Although exogenous intraocular application of BDNF provides neuroprotection to RGCs after axotomy, the endogenous increase in BDNF in the retina after 28 days of enrichment had no effect on RGC survival. While enriched housing conditions offer a model of non-invasive rehabilitation treatment for injury and modulates changes in BDNF and TrkB levels, these molecular changes did not translate into a neuroprotective effect on RGCs following transection of the optic nerve.

Original languageEnglish
Pages (from-to)1-11
Number of pages11
JournalBrain Research
Volume1095
Issue number1
DOIs
Publication statusPublished - 2006

Bibliographical note

Funding Information:
The authors would like to thank Dr. David Kaplan for generously providing the TrkB antibodies. This research is supported by the Nova Scotia Health Research Foundation (NSHRF), the Canadian Institutes for Health Research (CIHR) and the Department of Surgery at Dalhousie University. TBF was supported by a scholarship from the Nova Scotia Health Research Foundation.

ASJC Scopus Subject Areas

  • General Neuroscience
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

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