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

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 24h 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.