Kainate-induced toxicity in the hippocampus: potential role of lithium

摘要: Crespo-Biel N, Camins A, Canudas AM, Pallas M. Kainate-induced toxicity in the hippocampus: potential role of lithium. Bipolar Disord 2010: 12: 425–436. © 2010 The Authors. Journal compilation John Wiley & Sons A/S. Objectives:  We investigated neuroprotective effects lithium an experimental neurodegeneration model gated to kainate (KA) receptor activation. Methods:  hippocampus from KA-treated mice and hippocampal cell cultures were used evaluate pathways regulated by chronic pretreatment both vivo vitro models. Results:  Treatment with KA, as measured fragmentation α-spectrin biochemically, induced activation calpain resulting p35 cleavage p25, indicating cyclin-dependent kinase 5 (cdk5) glycogen synthase kinase-3s (GSK-3s) increase tau protein phosphorylation. reduced cdk5 GSK-3s on tau. KA treatment resulted neuronal demise. According nuclear condensed counts, addition (0.5–1 mM) a few days before had also antiapoptotic effects. action calpain/cdk5 produced similar results vivo. As is activated intracellular calcium, we showed that calcium concentrations basal cells, which was accompanied NCX3, Na+/Ca2+ exchanger pump. Conclusion:  A robust effect excitotoxic process mouse demonstrated via modulation entry subsequent inhibition pathway. These mechanisms may act additive way other previously described for lithium, suggesting it be useful possible therapeutic strategy Alzheimer’s disease.