Visualization of calcium signals in acute thromboembolic model of stroke

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The increase in intracellular calcium ion plays a pivotal in processing vital function. Both necrosis and apoptosis are triggered by the influx of calcium ion via plasma membrane. The stimuli, such as ischemia and trauma, enhance permeability of calcium ion through plasma membrane. The elevation of intracellular calcium ion activates various proteolytic enzymes and caspases. If the calcium ion level reaches high enough to cause cell dysfunction, either apoptosis or necrosis may be programmed. One can surmise that cell death may be prevented by the inhibition of calcium overload. However, distribution of calcium signals during cerebral ischemia has not yet been demonstrated. We developed a novel method to detect calcium signals in the rat cerebral cortex after thromboembolic ischemia. Exposed rat cerebral cortex was preloaded with fra-2 AM, then Rose Bengal was injected intravenously. The proximal middle cerebral artery was irradiated producing thrombosis with 540 nm wavelength green light. Thereafter, ischemic cerebral cortex was alternatively irradiated with 340 and 380 nm light to emit chemiluminescence. The intensity of chemiluminescence took a peak at 60 minutes after the alternative irradiation. The highest calcium signals occurred in ischemic core which was proved by the pathological examination. In ischemic penumbra calcium signal was moderate. No calcium signal was demonstrated in normal cortex. The region of ischemic penumbra deemed a therapeutic target of rescue from cell death. In conclusion, we demonstrated for the first time calcium signals in the ischemic cerebral cortex in vivo.