Samson Herman H, Cunningham Christopher L, Czachowski Cristine L, Chappell Ann, Legg Brooke, Shannon Erin
Center for the Neurobehavioral Study of Alcohol, Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC 27157-1083, USA.
Alcohol. 2004 Apr;32(3):203-12. doi: 10.1016/j.alcohol.2004.02.002.
Postingestive CNS pharmacologic effects of ethanol are often assumed to provide the major stimuli for development and maintenance of ethanol self-administration in rats. However, there is little direct evidence to support this assumption. In all procedures that have been used to initiate ethanol intake in rats, some type of taste adaptation or taste conditioning could account for the increased and maintained ethanol intake. Thus, it remains critical to demonstrate that increased ethanol intake is related to postingestive CNS actions of ethanol, and not to a positive shift in the hedonic taste value of the solution. Two experiments were performed to examine this question. In both studies, rats were trained to self-administer 20% ethanol by using a sucrose-substitution initiation procedure. The rats were required to press a lever 25 or 30 times to gain access to 20% ethanol for 20 min from a sipper tube. Once initiated, extinction sessions were used to determine the strength of ethanol seeking by measuring the number of lever presses that occurred in 20 min with no presentation of the ethanol solution. After initial training, the rats were split into two groups: one that received pairings of a gavage of ethanol (1 g/kg), followed after 10 min by a lithium chloride (LiCl) injection (paired group), and one that also received ethanol gavage and LiCl injections, but separated by 24 h (unpaired group). This pairing of postingestive effects with the illness induced by LiCl injection has been shown to devalue other food and fluid reinforcers. In Experiment 1, the rats received four pairings, one after the other with no behavioral testing between. In Experiment 2, the rats received three pairings and were tested for devaluation after each pairing. Results from both experiments showed significant decreases in seeking behavior in both groups, but seeking behavior was decreased significantly greater in the paired group, even though neither group had access to ethanol during the extinction testing periods. In Experiment 1, when ethanol became available after the devaluation procedure, the pattern of intake in the paired group was unchanged early in the sipper tube availability period, supporting the suggestion that the devaluation effect was not mediated by taste stimuli. These findings support the assumption that postingestive effects contribute to the reinforcement produced by self-administered ethanol in rats.
乙醇摄入后对中枢神经系统的药理作用通常被认为是大鼠乙醇自我给药行为发展和维持的主要刺激因素。然而,几乎没有直接证据支持这一假设。在所有用于启动大鼠乙醇摄入的实验程序中,某种类型的味觉适应或味觉条件作用可能是乙醇摄入量增加并维持的原因。因此,至关重要的是要证明乙醇摄入量的增加与乙醇摄入后对中枢神经系统的作用有关,而不是与溶液享乐味觉值的正向变化有关。进行了两项实验来研究这个问题。在这两项研究中,通过蔗糖替代启动程序训练大鼠自我给药20%的乙醇。大鼠需要按压杠杆25或30次,才能从吸管中获取20%的乙醇20分钟。一旦启动,采用消退实验来通过测量在20分钟内无乙醇溶液呈现时的杠杆按压次数来确定对乙醇的寻求强度。初始训练后,大鼠被分为两组:一组接受乙醇灌胃(1克/千克),10分钟后注射氯化锂(LiCl)(配对组),另一组也接受乙醇灌胃和LiCl注射,但间隔24小时(非配对组)。已证明这种摄入后效应与LiCl注射引起的疾病的配对会降低其他食物和液体强化物的价值。在实验1中,大鼠接受四次配对,每次配对后不进行行为测试。在实验2中,大鼠接受三次配对,并在每次配对后进行贬值测试。两项实验的结果均显示两组的寻求行为均显著下降,但配对组的寻求行为下降幅度更大,尽管在消退测试期间两组均无法获得乙醇。在实验1中,贬值程序后乙醇可用时,配对组在吸管可用期早期的摄入模式没有变化,这支持了贬值效应不是由味觉刺激介导的这一观点。这些发现支持了这样一种假设,即摄入后效应有助于大鼠自我给药乙醇产生的强化作用。