Kehoe P, Shoemaker W
Trinity College, Hartford, CT.
Pharmacol Biochem Behav. 1991 Jun;39(2):389-94. doi: 10.1016/0091-3057(91)90197-a.
Pregnant rats were given diets containing either 5% ethanol, an isocaloric (pair-fed) diet, or casein pellets. Offspring were tested at postnatal day 10 for isolation-induced ultrasonic vocalizations and subsequent stress-induced analgesia. Rats prenatally exposed to ethanol vocalized significantly less in the five minutes during isolation. The opiate, morphine, caused a greater suppression of vocalizations in alcohol-exposed pups compared to controls, while the increased calling normally seen with the opiate antagonist, naltrexone, was attenuated. In a test in which the pup withdraws a paw from a hot plate (48 degrees C), prenatal alcohol offspring demonstrated baseline latencies (no isolation) similar to controls but had greatly attenuated responses in their isolation-induced analgesia. Since both vocalization and analgesia responses have been determined to be modulated by the endogenous opioid system, the aberrant responses of the prenatal-ethanol-exposed offspring can be interpreted as failures to respond by opioid release/secretion to appropriate stimuli.
给怀孕的大鼠喂食含有5%乙醇的饮食、等热量(配对喂养)饮食或酪蛋白颗粒。在出生后第10天对后代进行测试,检测隔离诱导的超声波发声以及随后的应激诱导镇痛。产前暴露于乙醇的大鼠在隔离期间的五分钟内发声明显减少。与对照组相比,阿片类药物吗啡对暴露于酒精的幼崽的发声抑制作用更大,而通常在阿片类拮抗剂纳曲酮作用下增加的叫声则减弱。在一项幼崽将爪子从热板(48摄氏度)上撤回的测试中,产前暴露于酒精的后代在无隔离情况下的基线潜伏期与对照组相似,但在隔离诱导镇痛中的反应大大减弱。由于发声和镇痛反应都已被确定受内源性阿片系统调节,因此产前暴露于乙醇的后代的异常反应可解释为阿片类物质释放/分泌对适当刺激无反应。