Increased vulnerability to cocaine in mice lacking the serotonin-1B receptor
Increased vulnerability to cocaine in mice lacking the serotonin-1B receptor
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作者：
Rocha, BA;Scearce-Levie, K;Hen, R
越来越多的证据表明，遗传因素会影响对药物滥用的脆弱性的个体差异（1、2）。5-羟色胺（5-羟色胺，5-HT），通过许多受体起作用，可以调节神经奖励途径的活性，从而调节各种滥用药物的影响（3-8）。在这里，我们研究了可卡因对缺乏一种5-HT 1B受体亚型的小鼠的影响（9）。我们发现，缺乏5-HT 1B的小鼠对可卡因的运动反应增加，并且它们更有动力自我管理可卡因。我们认为，即使是药物幼稚的5-HT 1B基因敲除小鼠的行为和生化状态，类似于野生型小鼠反复暴露于药物对可卡因敏感。这种改变的状态可能是他们对可卡因的脆弱性增加的原因。
There is increasing evidence that genetic factors can influence individual differences in vulnerability to drugs of abuse(1,2). Serotonin (5-hydroxytryptamine, 5-HT), acting through many receptors can modulate the activity of neural reward pathways and thus the effects of various drugs of abuse(3-8). Here we examine the effects of cocaine in mice lacking one of the serotonin-receptor subtypes, the 5-HT1B receptor(9). We show that mice lacking 5-HT1B display increased locomotor responses to cocaine and that they are more motivated to self-administer cocaine. We propose that even drug-naive 5-HT1B-knockout mice are in a behavioural and biochemical state that resembles that of wild-type mice sensitized to cocaine by repeated exposure to the drug. This altered state might be responsible for their increased vulnerability to cocaine.