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Methionine-enkephalin and leucine-enkephalin increase interleukin-1 beta release in mixed glia cultures
Jan Kowalski1, Bozena Gabryel, Krzysztof Łabuzek
1Department of Clinical Pharmacology, Medical University of Silesia, Medyków, Poland. farmkin@infomed.slam.katowice.pl
Interleukin-1 beta (IL-1 beta) is synthesized in the brain in response to LPS. Excessive IL-1 beta expression is observed in neurodegenerative diseases. The aim of this study was to evaluate the effects of methionine-enkephalin (ME) and leucine-enkephalin (LE) on the baseline and LPS-activated release of IL-1 beta in rat mixed glia cultures. ME and LE increased LPS-induced IL-1 beta release, which was not blocked by naloxone. Both ME and LE increased the baseline release of IL-1 beta, which was completely blocked by naloxone pretreatment. Mixed glia cultures deprived of microglia (by shaking and incubating with L-leucine methyl ester) did not release IL-1 beta, which indicates microglia as a source of the changes in IL-1 beta release. The results of the study suggest that neurons may regulate glial activity through releasing enkephalins.
Interleukin-1 beta (IL-1 beta) is synthesized in the brain in response to LPS. Excessive IL-1 beta expression is observed in neurodegenerative diseases. The aim of this study was to evaluate the effects of methionine-enkephalin (ME) and leucine-enkephalin (LE) on the baseline and LPS-activated release of IL-1 beta in rat mixed glia cultures. ME and LE increased LPS-induced IL-1 beta release, which was not blocked by naloxone. Both ME and LE increased the baseline release of IL-1 beta, which was completely blocked by naloxone pretreatment. Mixed glia cultures deprived of microglia (by shaking and incubating with L-leucine methyl ester) did not release IL-1 beta, which indicates microglia as a source of the changes in IL-1 beta release. The results of the study suggest that neurons may regulate glial activity through releasing enkephalins.