Ischemic injury decreases parvalbumin expression in a middle cerebral artery occlusion animal model and glutamate-exposed HT22 cells

Neurosci Lett. 2012 Mar 14;512(1):17-21. doi: 10.1016/j.neulet.2012.01.044. Epub 2012 Jan 25.

Abstract

Parvalbumin is a calcium-binding albumin protein that is involved in neuronal maturation, differentiation, axonal transport, and neurotransmitter release. Parvalbumin protects neuron from cell death through reduction of intracellular Ca²⁺ concentrations. In this study, we investigated parvalbumin expression after neuronal cell injury. Middle cerebral artery occlusions (MCAO) were surgically performed in a rat model to induce focal cerebral ischemic injury. Adult male rats were used and brain tissues were collected 24 h after MCAO. MCAO increases infarct damages and apoptotic cell death in cerebral cortex. A proteomic approach revealed a decrease of parvalbumin expression in MCAO-operated animals. RT-PCR and Western blot analyses showed that MCAO induces a reduction in parvalbumin transcript and protein levels, respectively. The numbers of parvalbumin-positive cells were also decreased in the cerebral cortices of MCAO-operated animals. Moreover, glutamate exposure significantly increased intracellular Ca²⁺ concentrations and induced a reduction of parvalbumin expression in a hippocampal-derived cell line. These results suggest that the reduction in parvalbumin levels after ischemic brain injury can modulate neuronal cell death.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • Cell Survival / drug effects
  • Disease Models, Animal
  • Glutamic Acid / toxicity
  • Infarction, Middle Cerebral Artery / metabolism*
  • Infarction, Middle Cerebral Artery / pathology
  • Male
  • Mice
  • Neurons / cytology
  • Neurons / drug effects
  • Neurons / metabolism
  • Parvalbumins / metabolism*
  • Rats
  • Rats, Sprague-Dawley

Substances

  • Parvalbumins
  • Glutamic Acid