GENERAL, MU AND KAPPA-OPIOID ANTAGONISTS IN THE NUCLEUS-ACCUMBENS ALTER FOOD-INTAKE UNDER DEPRIVATION, GLUCOPRIVIC AND PALATABLE CONDITIONS
GENERAL, MU AND KAPPA-OPIOID ANTAGONISTS IN THE NUCLEUS-ACCUMBENS ALTER FOOD-INTAKE UNDER DEPRIVATION, GLUCOPRIVIC AND PALATABLE CONDITIONS
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DOI：
10.1016/0006-8993(95)00957-r
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发表时间：
1995-11-27
期刊：
影响因子：
2.9
通讯作者：
COOPER, ML
中科院分区：
文献类型：
--
作者：
BODNAR, RJ;GLASS, MJ;COOPER, ML
脑室微量注射研究发现，μ（β - 氟纳曲胺，B - FNA）、μ₁（纳洛酮嗪）和κ（去甲二氢-β - 刺桐若碱，Nor - BNI）阿片受体拮抗剂，但不是δ拮抗剂，可减少剥夺诱导的摄入；κ和μ，但不是μ₁或δ拮抗剂可减少2 - 脱氧 - D - 葡萄糖（2DG）诱导的多食和蔗糖摄入。由于阿片激动剂刺激伏隔核的自发食物摄入，本研究检测了在伏隔核给予纳曲酮、B - FNA或Nor - BNI是否会改变剥夺（24小时）、糖剥夺（2DG：500 mg/kg，腹腔注射）或可口蔗糖（10%）条件下的摄入。还评估了纳洛酮嗪在伏隔核对剥夺诱导摄入的影响。在伏隔核中，纳曲酮（5 - 20μg，44%）、B - FNA（1 - 4μg，55%）和Nor - BNI（4μg，31%）在4小时内显著降低了剥夺诱导的摄入，但纳洛酮嗪（10μg）没有此作用。在伏隔核中，纳曲酮（10 - 20μg，79%）、B - FNA（1 - 4μg，100%）和Nor - BNI（1 - 4μg，75%）显著降低了2DG诱导的多食。在伏隔核中，纳曲酮（50μg，27%）和B - FNA（1 - 4μg，37%）显著降低了蔗糖摄入，但Nor - BNI没有。这些数据表明，伏隔核中的μ受体，特别是μ₂结合位点负责该核中这些摄入形式的阿片调节，并且这种控制可能作用于摄入本身的量。
Ventricular microinjection studies found that whereas mu(beta-funaltrexamine, B-FNA), mu(1) (naloxonazine) and kappa (nor-binaltorphamine, Nor-BNI) opioid receptor antagonists, but not delta antagonists, reduce deprivation-induced intake, kappa and mu, but not mu(1) or delta antagonists reduce both 2-deoxy-D-glucose (2DG) hyperphagia and sucrose intake. Since opioid agonists stimulate spontaneous food intake in the accumbens, the present study examined whether administration of either naltrexone, B-FNA or Nor-BNI in the accumbens altered intake under deprivation (24 h), glucoprivic (2DG: 500 mg/kg, i.p.) or palatable sucrose (10%) conditions. Naloxonazine's effects in the accumbens were also evaluated for deprivation-induced intake. Deprivation-induced intake was significantly decreased over 4 h by naltrexone (5-20 mu g, 44%), B-FNA (1-4 mu g, 55%) and Nor-BNI (4 mu g, 31%), but not naloxonazine (10 mu g) in the accumbens. 2DG hyperphagia was significantly decreased by naltrexone (10-20 mu g, 79%), B-FNA (1-4 mu g, 100%) and Nor-BNI(1-4 mu g, 75%) in the accumbens. Sucrose intake was significantly decreased by naltrexone (50 mu g, 27%) and B-FNA (1-4 mu g, 37%), but not Nor-BNI in the accumbens. These data suggest that mu receptors, and particularly the mu(2) binding site in the accumbens are responsible for the opioid modulation of these forms of intake in this nucleus, and that this control may be acting upon the amount of intake per se.