Cerebral system is a pathology with important social and economical consequences. Several evidences have suggested that an increase in the extracellular concentration of glutamate is involved in the cellular damage observed after cerebral ischemia. Glutamate will overstimulate the NMDA receptor causing a dramatic influx of calcium inside the neurons and the production of free radicals. The manipulation of the mechanisms involved in the control of glutamate release or the NMDA excitabily are genuine therapeutic targets to decrease the cellular damage caused by ischemia. In this respect, we will investigate whetherhistamine potentiates or reduce the hypoxia/hipoglucemia cellular death by acting at the level glutamate release and/or NMDA receptor stimulation. On the other hand, it is becoming apparent that apoptotic death does occur in cerebral ischemia. We will then study the involvement of the ceramide synthesis and the activation caspases in the neuronal death caused by hypoxia/hipoglucemia. The eventual implication of NMDA receptors in the ceramide pathway will be also tested.
|Effective start/end date||1/07/98 → 1/07/01|
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