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This study sought to elucidate the precise mechanisms of DBI mRNA up\u2010regulation by long\u2010term treatment with morphine using primary cultures of mouse cerebral cortical neurons. A significant increase in DBI mRNA was observed after sustained exposure to 0.3 \u03bcM morphine for 2 days, and the maximal expression occurred after 2 days of exposure, whereas transient exposure to 0.3 \u03bcM morphine for 15 min, 1 hr, and 3 hr produced no changes in the expression. Continuous exposure to DAMGO also significantly increased DBI mRNA expression, which was completely abolished by a selective antagonist of \u03bc\u2010opioid receptors, \u03b2\u2010funaltrexamine (\u03b2\u2010FNA). The morphine\u2010induced increase in DBI mRNA expression and its content were completely inhibited by naloxone and \u03b2\u2010FNA, and the inhibitory potential of naloxonazine was about half that of \u03b2\u2010FNA. On the other hand, \u03ba\u2010 and \u03b4\u2010opioid receptor antagonists showed no effects on the morphine\u2010induced increase in DBI mRNA. In addition, both a calmodulin antagonist and a CaM II kinase inhibitor significantly suppressed the morphine\u2010induced increase in DBI mRNA. These results indicate that the increase in DBI expression is induced by continuous activation of \u03bc\u2010opioid receptors but not of \u03ba\u2010 and \u03b4\u2010opioid receptors and is regulated by the calcium\/calmodulin\u2010related phosphorylation system. \u00a9 2007 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.21415","type":"journal-article","created":{"date-parts":[[2007,7,17]],"date-time":"2007-07-17T00:56:32Z","timestamp":1184633792000},"page":"2971-2980","source":"Crossref","is-referenced-by-count":4,"title":["Increase in diazepam binding inhibitor expression by sustained morphine exposure is mediated via \u03bc\u2010opioid receptors in primary cultures of mouse cerebral cortical 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