Abstract
In HEK293 cells stably expressing α4β2 nAChRs, naltrexone, but not naloxone, blocked α4β2 nAChRs via an open-channel blocking mechanism. In primary hippocampal cultures, naltrexone inhibited α7 nAChRs up-regulated by nicotine, and in organotypic hippocampal cultures naltrexone caused a time-dependent up-regulation of functional α7 nAChRs that was detected after removal of the drug. These results indicate that naltrexone could be used as a smoking cessation aid.
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