Frankel D, Khanna J M, Kalant H, Leblanc A E
Psychopharmacology (Berl). 1978 Mar 1;56(2):139-43. doi: 10.1007/BF00431839.
Rats were rendered tolerant to the motor-impairing effects of ethanol by daily oral administration. Subsequently, ethanol was withdrawn and the effect of p-chlorophenylalanine (p-CPA) on tolerance loss was examined. In two separate studies it was demonstrated that p-CPA, in a dosage regimen that produces extensive depletion of brain serotonin (5-HT), accelerated tolerance loss. These experiments suggest that at least part of p-CPA's inhibitory effect on net tolerance development to ethanol can be accounted for by its accelerating effect on tolerance loss; however, an inhibitory effect on tolerance acquisition cannot be excluded. On the other hand, once tolerance was established, p-CPA did not affect the maintenance of tolerance to ethanol.
通过每日口服给药使大鼠对乙醇的运动损害作用产生耐受性。随后，停止给予乙醇，并检测对氯苯丙氨酸（p-CPA）对耐受性丧失的影响。在两项独立研究中表明，p-CPA以能使脑血清素（5-HT）大量耗竭的剂量方案加速了耐受性丧失。这些实验表明，p-CPA对乙醇净耐受性发展的抑制作用至少部分可归因于其对耐受性丧失的加速作用；然而，对耐受性获得的抑制作用也不能排除。另一方面，一旦建立耐受性，p-CPA并不影响对乙醇耐受性的维持。
