Study on the glutamate-induced spinal neurodysfunction.

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In this study, we investigated mechanisms underlying the dysfunction of glutamate transmission under the inflammatory condition in the spinal cord. We also examined effects of drugs acting on CNS functions. We made in vitro inflammation model using co-culture comprised of astrocytes, microglia and neurons obtained from newborn rat brains. Inflammation decreased glutamate transport by down-regulation of GLAST induced by high-concentration of extracellular glutamate released from activated microglia in this co-culture. Among centrally acting drugs including antidepressants we tested, only paroxetine inhibited the inflammation-induced glutamate release from activated microglia and prevented the decrease in the glutamate transport. We also demonstrated that ATP is one of the factor that made the neural inflammation worse.