Social learning about ethanol in preweanling rats: role of endogenous opioids.
Social learning about ethanol in preweanling rats: role of endogenous opioids.
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断奶前大鼠关于乙醇的社会学习：内源性阿片类药物的作用。
DOI：
10.1002/dev.10163
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发表时间：
2004
影响因子：
2.2
通讯作者：
Hunt,PamelaS
中科院分区：
文献类型：
--
作者：
Hallmark,RachelA;Hunt,PamelaS
内源性阿片系统的作用，在社会学习的乙醇进行了检查，在三个实验中使用断奶前大鼠。实验1表明，在出生后第12天（PD），14日和16日的家庭笼中与中毒的兄弟姐妹的相互作用，结果增加自愿摄入乙醇时，受试者进行测试后24小时，最终曝光。结果还表明，内源性阿片系统不参与习得。在社会暴露于乙醇期间给予纳洛酮对以后的乙醇摄入量没有影响。实验2检查了试验前给予的受体选择性拮抗剂的作用。对于社会暴露于乙醇的受试者，纳洛酮或δ拮抗剂纳曲吲哚完全抑制了乙醇的摄入。对于乙醇初治受试者，纳洛酮也完全抑制了摄入量。然而，纳曲吲哚或μ拮抗剂β-FNA可部分阻断摄入。实验3通过对β-FNA和纳曲吲哚进行更全面的剂量反应分析，证实了μ和δ受体在乙醇摄入中的差异参与。总的来说，这些数据表明，从中毒的同种了解乙醇不仅会影响自愿摄入乙醇，但也改变了阿片类药物对乙醇消费的反应。© 2004 Wiley Periodicals，Inc. Dev Psychobiol 44：132-139，2004.
The role of the endogenous opioid system in social learning about ethanol was examined in three experiments using preweanling rats. Experiment 1 showed that interactions with intoxicated siblings in the home cage on postnatal Days (PD) 12, 14, and 16 results in increased voluntary intake of ethanol when subjects are tested 24 hr after the final exposure. The results also suggested that the endogenous opioid system is not involved in acquisition. Administration of naloxone during social exposure to ethanol had no effect on later ethanol intake. Experiment 2 examined the effects of receptor‐selective antagonists administered prior to test. For subjects that had social exposure to ethanol, intake of ethanol was completely suppressed by either naloxone or the δ antagonist naltrindole. For ethanol‐naïve subjects, intake also was completely suppressed by naloxone. However, intake was partially blocked by naltrindole or the μ antagonist β‐FNA. Experiment 3 confirmed the differential involvement of μ and δ receptors in ethanol intake through a more comprehensive dose–response analysis of β‐FNA and naltrindole. Collectively, these data reveal that learning about ethanol from intoxicated conspecifics not only affects voluntary intake of ethanol but also alters the opioidergic response to ethanol consumption. © 2004 Wiley Periodicals, Inc. Dev Psychobiol 44: 132–139, 2004.
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