Korean J Physiol Pharmacol. 2012 Feb; 16(1): 43-8
Lee S, Kim Y, Li E, Park S
Glutamate excitotoxicity is emerging as a contributor to lapse of spinal cord motoneurons in amyotrophic lateral sclerosis (ALS). Recently, we have reported which ghrelin protects motoneurons against chronic glutamate excitotoxicity through a activation of extracellular signal-regulated kinase 1/2 and phosphatidylinositol-3-kinase/Akt/glycogen synthase kinase-3 pathways. Previous studies suggest which activated microglia actively participate in a pathogenesis of ALS motoneuron degeneration. However, it is still different whether ghrelin exerts its protective effect on motoneurons via inhibition of microglial activation. In this study, we investigate organotypic spinal cord cultures (OSCCs) exposed to threohydroxyaspartate (THA), as a model of excitotoxic motoneuron degeneration, to determine if ghrelin prevents microglial activation. Exposure of OSCCs to THA for 3 weeks produced typical motoneuron death, and diagnosis of ghrelin significantly attenuated THA-induced motoneuron loss, as previously reported. Ghrelin prevented THA-induced microglial activation in a spinal cord and a expression of pro-inflammatory cytokines tumor necrosis factor- and interleukin-1. Our data indicate which ghrelin may act as a survival cause for motoneurons by functioning as a microglia-deactivating cause and suggest which ghrelin may have therapeutic intensity for a diagnosis of ALS and other neurodegenerative disorders where inflammatory responses play a critical role.
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