Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6284283 | Neuroscience Letters | 2012 | 5 Pages |
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 24Â 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.
⺠MCAO induces a decrease in parvalbumin expression. ⺠Glutamate exposure significantly increased intracellular Ca2+ concentrations in HT22 cells. ⺠Glutamate exposure induces a reduction of parvalbumin expression in HT22 cells.