Tyrosine kinase A but not phosphacan/protein tyrosine phosphatase-zeta/beta immunoreactivity and protein level changes in neurons and astrocytes in the gerbil hippocampus proper after transient forebrain ischemia

Brain Res. 2005 Mar 2;1036(1-2):35-41. doi: 10.1016/j.brainres.2004.12.037.

Abstract

In the present study, ischemia-related changes in tyrosine kinase A (trkA) and phosphacan/protein tyrosine phosphatase-zeta/beta (PTP-zeta/beta) immunoreactivities and protein contents were examined in the hippocampus proper after transient forebrain ischemia for 5 min in a gerbil model. Our investigations showed that ischemia-induced changes occurred in trkA immunoreactivity in the hippocampal CA1 region, but not in the CA2/3 region of the hippocampus proper. In the sham-operated group, trkA immunoreactivity was barely detectable. trkA immunoreactivity increased from 30 min after ischemia and peaked at 12 h. Four days after ischemic insult, trkA immunoreactivity was observed in GFAP-immunoreactive astrocytes in the strata oriens and radiatum. In addition, we found that ischemia-related changes in trkA protein content were similar to immunohistochemical changes. On the other hand, PTP-zeta/beta immunoreactivities in the hippocampus proper were unaltered by forebrain ischemia. These results suggest that chronological changes of trkA after transient forebrain ischemia may be associated with an ischemic damage compensatory mechanism in CA1 pyramidal cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptation, Physiological / physiology
  • Animals
  • Astrocytes / enzymology*
  • Cell Survival / physiology
  • Cerebral Infarction / metabolism
  • Cerebral Infarction / physiopathology
  • Chondroitin Sulfate Proteoglycans / metabolism*
  • Disease Models, Animal
  • Gerbillinae
  • Glial Fibrillary Acidic Protein / metabolism
  • Hippocampus / enzymology*
  • Hippocampus / physiopathology
  • Immunohistochemistry
  • Ischemic Attack, Transient / enzymology*
  • Ischemic Attack, Transient / physiopathology
  • Male
  • Nerve Degeneration / metabolism
  • Nerve Degeneration / physiopathology
  • Nerve Tissue Proteins / metabolism*
  • Neurons / enzymology*
  • Protein Isoforms / metabolism
  • Protein Tyrosine Phosphatases / metabolism*
  • Pyramidal Cells / enzymology
  • Receptor, trkA / metabolism*
  • Receptor-Like Protein Tyrosine Phosphatases, Class 5
  • Time Factors
  • Up-Regulation / physiology

Substances

  • Chondroitin Sulfate Proteoglycans
  • Glial Fibrillary Acidic Protein
  • Nerve Tissue Proteins
  • Protein Isoforms
  • Receptor, trkA
  • Protein Tyrosine Phosphatases
  • Receptor-Like Protein Tyrosine Phosphatases, Class 5