초록
Data from our laboratory indicate that application of the mu agonist DAMGO into the basolateral complex of amygdala (BLA) suppresses tail flick reflexes in anesthetized rats. This DAMGO-induced antinociception can be blocked by pretreatment of the BLA with the nonselective opioid antagonist naltrexone, the mu opioid antagonist β-FNA, or the G protein inhibitor pertussis toxin, suggesting that DAMGO's interaction with G protein-coupled mu receptors in the BLA leads to production of antinociception. The present study employing the gene control strategy was conducted to further investigate the direct action of DAMGO on the mu receptors in the BLA. Intra-BLA application of antisense oligodeoxynucleotides (ODN) against mu receptors blocked antinociception following intra-BLA injection of DAMGO. The amount of [3H]-DAMGO binding to mu receptors in the amygdala was also reduced in the antisense ODN-pretreated rats. These data confirm the idea that antinociception induced by DAMGO in the BLA results from a direct interaction of DAMGO with mu receptors in the amygdala.
키워드
Mu receptor; Amygdala; Tail flick; Gene control; Antisense oligodeoxynucleotides (ODN); [3H]-DAMGO binding
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