Very delayed neuronal loss occurs in the glomerular layer of the main olfactory bulb following transient ischemia in gerbils

Neurosci Lett. 2004 Aug 19;366(3):272-6. doi: 10.1016/j.neulet.2004.05.071.

Abstract

Olfactory dysfunction could happen following various insults such as ischemic-hypoxic state. Neurons of the main olfactory bulb (MOB) are resistant to ischemic damage. In the present study, we investigated the ischemia-related changes of neurons and glial cells in the glomerular layer (GL) of the gerbil MOB after transient ischemia. The number of NeuN-immunoreactive neurons became to decrease from 10 days after ischemic insult. Fifteen days after ischemic insult, astrocytes and microglia were increased in number. By 60 days after ischemia, NeuN-immunoreactive neurons were significantly decreased by 42% per glomerulus. At this time period, astrocytes and microglia were pronouncedly increased. This result indicates that neuronal loss must be much delayed in the GL following transient ischemia.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • CD11b Antigen / metabolism
  • Cell Count / methods
  • Cell Death
  • Gerbillinae
  • Glial Fibrillary Acidic Protein / metabolism
  • Immunohistochemistry / methods
  • Ischemic Attack, Transient / metabolism
  • Ischemic Attack, Transient / pathology*
  • Male
  • Nerve Degeneration
  • Neuroglia / metabolism
  • Neurons / pathology*
  • Olfactory Bulb / pathology*
  • Phosphopyruvate Hydratase / metabolism
  • Time Factors

Substances

  • CD11b Antigen
  • Glial Fibrillary Acidic Protein
  • Phosphopyruvate Hydratase