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苯丙胺或苯环利定的延迟效应:食物剥夺、应激与剂量的相互作用

Delayed effects of amphetamine or phencyclidine: interaction of food deprivation, stress and dose.

作者信息

Coveney J R, Sparber S B

机构信息

Department of Pharmacology, University of Minnesota, Minneapolis 55455.

出版信息

Pharmacol Biochem Behav. 1990 Jul;36(3):443-9. doi: 10.1016/0091-3057(90)90239-e.

DOI:10.1016/0091-3057(90)90239-e
PMID:2377646
Abstract

Tritium-labelled phencyclidine (PCP) hydrochloride (12 mg/kg) was injected SC for six consecutive days into two groups of eight male rats maintained at 85% of their initial free-feeding weights. Eight days after the last injection, electric footshock raised fat levels of PCP 28% over nonshocked controls, and lowered blood levels 18%, but did not alter brain levels of the drug significantly. Thus, application of an acute stressor does result in redistribution of tissue stores of phencyclidine as predicted in the literature; however, the direction of the redistributions was to fat, rather than to brain. To explore the relation of a long-term stressor (one that eliminates adipose tissue as a sink for mobilized PCP), exploratory behavior was evaluated in male rats during six days of food deprivation commencing after six daily injections of PCP HCl (2 or 4 mg/kg, SC). Exploratory behavior of the 4 mg/kg dose group was abruptly altered, compared to saline controls, at six days of food deprivation, when the rats' body weights were about 70% of initial weights and when body fat would be severely reduced or depleted. To assess replicability and generalizability of this phenomenon, PCP HCl (4 or 8 mg/kg, SC) or dextroamphetamine sulfate (3.2 or 6.4 mg/kg, SC) was injected into male rats for six days and food deprivation followed afterward for nine consecutive days, or until similar body weight reductions as in the first experiment were achieved. Again, exploratory behavior was altered in comparison to saline controls in phencyclidine-treated rats (at the 4 mg/kg dose level) when rats reached about 70% of initial weights.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

将盐酸氚标记的苯环己哌啶(PCP)(12毫克/千克)皮下注射给两组各八只雄性大鼠,连续六天,大鼠维持在其初始自由摄食体重的85%。最后一次注射八天后,电击足部使PCP的脂肪水平比未受电击的对照组提高了28%,血液水平降低了18%,但未显著改变药物的脑内水平。因此,急性应激源的应用确实会导致苯环己哌啶的组织储存重新分布,正如文献中所预测的那样;然而,重新分布的方向是脂肪,而非大脑。为了探究长期应激源(一种消除脂肪组织作为动员的PCP储存库的应激源)的关系,在雄性大鼠连续六天皮下注射盐酸PCP(2或4毫克/千克)后开始的六天食物剥夺期间,评估其探究行为。与生理盐水对照组相比,4毫克/千克剂量组的探究行为在食物剥夺六天时突然改变,此时大鼠体重约为初始体重的70%,且体脂会严重减少或耗尽。为了评估这一现象的可重复性和普遍性,将盐酸PCP(4或8毫克/千克,皮下注射)或硫酸右苯丙胺(3.2或6.4毫克/千克,皮下注射)注射给雄性大鼠六天,随后连续九天进行食物剥夺,或直至体重减轻程度与第一个实验相似。同样,当大鼠体重达到初始体重的约70%时,与生理盐水对照组相比,接受苯环己哌啶治疗的大鼠(4毫克/千克剂量水平)的探究行为发生了改变。(摘要截断于250字)

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