Dougherty Donald M, Marsh Dawn M, Mathias Charles W, Dawes Michael A, Bradley Don M, Morgan Chris J, Badawy Abdulla A-B
Neurobehavioral Research Laboratory and Clinic, Department of Psychiatry and Behavioral Medicine, Wake Forest University Health Sciences, Medical Center Boulevard, Winston-Salem, NC 27157, USA.
Psychopharmacology (Berl). 2007 Jul;193(1):137-50. doi: 10.1007/s00213-007-0763-6. Epub 2007 Mar 22.
Indirect evidence supports a link between serotonergic activity and individual differences in the behavioral response to alcohol, but few studies have experimentally demonstrated that an individual's biological state can influence the sensitivity to alcohol-induced behaviors.
Our purpose was to temporarily modify serotonin synthesis in healthy individuals to determine how altered biological states may interact with alcohol administration to affect impulsive behavior.
In a repeated-measures design, 18 normal controls consumed a 50-g L: -tryptophan (Trp) depleting (ATD) or loading (ATL) amino-acid beverage that temporarily decreased or increased (respectively) serotonin synthesis before receiving either a moderate dose of alcohol (0.65 g/kg) or placebo. All participants completed three impulsivity testing sessions on each of the five experimental days. Session one was a baseline session. Session two included testing after ATD-only or ATL-only. Session three included: (1) placebo after ATL (ATL+PBO); (2) placebo after ATD (ATD+PBO); (3) alcohol after ATL (ATL+ALC); (4) alcohol after ATD (ATD+ALC); and (5) Alcohol-only conditions. Impulsivity was assessed using the Immediate Memory Task (Dougherty et al., Behav Res Methods Instrum Comput 34:391-398, 2002), a continuous performance test yielding commission errors that have been previously validated as a component of impulsive behavior.
Primary findings were that ATD-only increased impulsive responding compared to ATL-only, and ATD+ALC increased commission errors to levels higher than either the ATL+ALC or Alcohol-only conditions.
These findings demonstrate that reduced serotonin synthesis can produce increased impulsivity even among non-impulsive normal controls, and that the behavioral effects of alcohol are, in part, dependent on this biological state.
间接证据支持血清素能活性与酒精行为反应的个体差异之间存在联系，但很少有研究通过实验证明个体的生物学状态会影响对酒精诱导行为的敏感性。
我们的目的是暂时改变健康个体的血清素合成，以确定改变的生物学状态如何与酒精给药相互作用来影响冲动行为。
在重复测量设计中，18名正常对照者饮用一种50克的L-色氨酸（Trp）消耗（ATD）或负荷（ATL）氨基酸饮料，该饮料在接受中等剂量酒精（0.65克/千克）或安慰剂之前分别暂时降低或增加血清素合成。所有参与者在五个实验日中的每一天都完成了三次冲动性测试。第一次测试是基线测试。第二次测试包括仅ATD或仅ATL后的测试。第三次测试包括：（1）ATL后服用安慰剂（ATL + PBO）；（2）ATD后服用安慰剂（ATD + PBO）；（3）ATL后服用酒精（ATL + ALC）；（4）ATD后服用酒精（ATD + ALC）；以及（5）仅酒精条件。使用即时记忆任务（Dougherty等人，《行为研究方法、仪器与计算机》34:391 - 398，2002）评估冲动性，这是一种连续执行测试，产生的错误率已被先前验证为冲动行为的一个组成部分。
主要发现是，仅ATD与仅ATL相比增加了冲动反应，并且ATD + ALC将错误率提高到高于ATL + ALC或仅酒精条件的水平。
这些发现表明，即使在非冲动性的正常对照者中，血清素合成减少也会导致冲动性增加，并且酒精的行为效应部分取决于这种生物学状态。
