Nogo-A is involved in secondary axonal degeneration of thalamus in hypertensive rats with focal cortical infarction

Neurosci Lett. 2007 May 7;417(3):255-60. doi: 10.1016/j.neulet.2007.02.080. Epub 2007 Mar 12.

Abstract

We investigate whether Nogo-A is involved in the secondary axonal degeneration in the thalamus after distal middle cerebral artery occlusion (MCAO) in stroke-prone renovascular hypertensive rats (RHRSP). The expression of Nogo-A in ipsilateral ventroposterior nucleus (VPN) of the thalamus in RHRSP was observed at 1, 2 and 4 weeks after distal MCAO. In addition, intracerebroventricular infusion of NEP1-40, a Nogo-66 receptor (NgR) antagonist peptide, was administered starting 24 h after MCAO and continued for 1, 2 and 4 weeks, respectively. Axonal damage and regeneration were evaluated by analysis of the immunoreactivity (IR) of amyloid betaA4 precursor protein (APP), growth associated protein 43 (GAP-43) and microtubule associated protein 2 (MAP-2) in ipsilateral VPN of the thalamus at 1, 2 and 4 weeks after distal MCAO. Following ischemia, the expression of Nogo-A in oligodendrocytes increased persistently and its localization became redistributed around damaged axons and dendrites. Administration of NEP1-40 downregulated the expression of Nogo-A, reduced axonal injury and enhanced axonal regeneration. Our data suggest that Nogo-A is involved in secondary axonal degeneration and that inhibition of Nogo-A can reduce neuronal damage in the thalamus after distal MCAO.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Axons / metabolism
  • Axons / pathology
  • Biomarkers / metabolism
  • Cerebral Infarction / metabolism*
  • Cerebral Infarction / pathology
  • Cerebral Infarction / physiopathology
  • Hypertension / complications*
  • Hypertension / physiopathology
  • Immunohistochemistry
  • Infarction, Middle Cerebral Artery / metabolism
  • Infarction, Middle Cerebral Artery / pathology
  • Infarction, Middle Cerebral Artery / physiopathology
  • Male
  • Myelin Proteins / metabolism*
  • Myelin Proteins / pharmacology
  • Myelin Proteins / therapeutic use
  • Nerve Growth Factors / pharmacology
  • Nerve Growth Factors / therapeutic use
  • Nerve Regeneration / drug effects
  • Nerve Regeneration / physiology
  • Nerve Tissue Proteins / metabolism
  • Nogo Proteins
  • Oligodendroglia / metabolism
  • Peptide Fragments / pharmacology
  • Peptide Fragments / therapeutic use
  • Rats
  • Rats, Sprague-Dawley
  • Retrograde Degeneration / metabolism*
  • Retrograde Degeneration / pathology
  • Retrograde Degeneration / physiopathology
  • Thalamus / metabolism*
  • Thalamus / pathology
  • Thalamus / physiopathology
  • Up-Regulation / physiology
  • Ventral Thalamic Nuclei / metabolism
  • Ventral Thalamic Nuclei / pathology
  • Ventral Thalamic Nuclei / physiopathology
  • Wallerian Degeneration / metabolism*
  • Wallerian Degeneration / pathology
  • Wallerian Degeneration / physiopathology

Substances

  • Biomarkers
  • Myelin Proteins
  • NEP1-40 protein, human
  • Nerve Growth Factors
  • Nerve Tissue Proteins
  • Nogo Proteins
  • Peptide Fragments
  • RTN4 protein, human
  • Rtn4 protein, rat