Mercaptoacetate induces feeding through central opioid-mediated mechanisms in rats.
Mercaptoacetate induces feeding through central opioid-mediated mechanisms in rats.
复制标题
巯基乙酸盐通过中枢阿片类药物介导的机制诱导大鼠进食。
DOI：
10.1016/s0006-8993(00)02162-4
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发表时间：
2000
期刊：
影响因子：
2.9
通讯作者：
Bodnar,RJ
中科院分区：
文献类型：
--
作者：
Stein,JA;Znamensky,V;Baumer,F;Rossi,GC;Pasternak,GW;Bodnar,RJ
内源性阿片样物质系统参与调节啮齿类动物的食物摄入，这些调节挑战如2-脱氧-D-葡萄糖（2DG）诱导的葡萄糖缺乏或食物剥夺。游离脂肪酸氧化抑制剂巯基乙酸（MA）的管理，产生了一个强大的短期增加大鼠的喂养，其机制已被解离引起的2DG。本研究通过全身给予阿片受体拮抗剂纳洛酮，通过中枢给予阿片受体拮抗剂μ、μ1、κ 1或δ，以及通过中枢给予针对μ（莫尔-1）、κ（KOR-1）、κ3（KOR-3/ORL-1）或δ（DOR-1）阿片受体克隆。全身性纳洛酮（0.005-5 mg/kg）可显著且剂量依赖性地降低MA诱导的摄食;这些摄食效应具有相当的选择性，因为MA本身或MA与纳洛酮配对均不影响总活动、行走活动或刻板活动。通过中枢预处理纳洛酮（0.1-20 μg）或μ-选择性（β-funalcidamine，0.1-20 μg）、μ1-选择性（纳洛嗪，1-20 μ g）、κ1-选择性（nor-binaltorphamine，0.1-20 μg）或δ-选择性（纳曲吲哚，1-20 μg）阿片受体拮抗剂，MA诱导的摄食显著减少。针对莫尔-1克隆的外显子1、2或3但不针对外显子4、针对KOR-1克隆的外显子3但不针对外显子1或2、针对KOR-3/ORL-1克隆的外显子1或2但不针对外显子3、针对DOR-1克隆的外显子1但不针对外显子2或3的AS ODN探针显著降低MA诱导的摄食。这些数据进行了讨论，在阿片类药物介导的摄食反应有关的脂肪，并在潜在的中央网站的行动，在该lipoprivic摄食反应可能采取行动。
The endogenous opioid system has been implicated in the mediation of food intake elicited by such regulatory challenges as glucoprivation induced by 2-deoxy-d-glucose (2DG) or food deprivation in rodents. Administration of the free fatty acid oxidation inhibitor, mercaptoacetate (MA), produces a potent short-term increase in feeding in rats, the mechanisms of which have been dissociated from that elicited by 2DG. The present study evaluated whether MA-induced feeding in rats was mediated by the endogenous opioid system through systemic administration of the general opioid antagonist, naltrexone, through central administration of either general, μ, μ1, κ1or δ opioid antagonists, and through central administration of antisense oligodeoxynucleotide (AS ODN) probes directed against specific exons of either the μ (MOR-1), κ (KOR-1), κ3(KOR-3/ORL-1) or δ (DOR-1) opioid receptor clones. MA-induced feeding was significantly and dose-dependently reduced by systemic naltrexone (0.005–5 mg/kg); these ingestive effects were quite selective since neither total, ambulatory nor stereotypic activity was affected by either MA itself or MA paired with naltrexone. MA-induced feeding was significantly reduced by central pretreatment with either naltrexone (0.1–20 μg) or μ-selective (β-funaltrexamine, 0.1–20 μg), μ1-selective (naloxonazine, 1–20 μg), κ1-selective (nor-binaltorphamine, 0.1–20 μg), or δ-selective (naltrindole, 1–20 μg) opioid receptor antagonists. MA-induced feeding was significantly reduced by AS ODN probes directed against either exons 1, 2 or 3, but not exon 4 of the MOR-1 clone, exon 3, but not exons 1 or 2 of the KOR-1 clone, exons 1 or 2, but not exon 3 of the KOR-3/ORL-1 clone, and exon 1, but not exons 2 or 3 of the DOR-1 clone. These data are discussed in terms of opioid mediation of ingestive responses related to fat, and in terms of potential central sites of action at which lipoprivic ingestive responses might act.