The role of nucleus accumbens adenosine-opioid interaction in mediating palatable food intake.
The role of nucleus accumbens adenosine-opioid interaction in mediating palatable food intake.
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DOI：
10.1016/j.brainres.2009.09.115
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发表时间：
2010-01-08
期刊：
影响因子：
2.9
通讯作者：
Will, Matthew J.
中科院分区：
文献类型：
--
作者：
Pritchett, Carolyn E.;Pardee, Alicia L.;McGuirk, Sophia R.;Will, Matthew J.
阿片样物质刺激可导致高可口食物的摄入量大幅增加，例如高脂肪饮食。虽然阿片类药物和这种现象背后的某些纹状体神经递质之间的相互作用已被探索，但许多潜在的相互作用还没有。研究表明，纹状体腺苷对纹状体神经传递和运动活动行为有显着影响，但阿片类药物和腺苷之间对进食行为的相互作用却很少受到关注。本研究在阿片类药物驱动的高脂肪饮食消费的背景下探讨了这种相互作用。具体地，检查了选择性A1和A2 A腺苷受体配体的内给药，同时或不同时给药μ-阿片激动剂DAla 2，N，Me-Phe 4，Gly-ol 5-enkaphalin（DAMGO），对高脂肪消耗和相关运动活性的影响。A1受体激动剂2-氯-N6-环戊基腺苷（CCPA）对基线或DAMGO诱导的运动或与高脂饮食相关的消费行为没有影响。然而，A2 A受体激动剂2-对-（2-羧乙基）-苯乙氨基-5 ′-N-乙基甲酰氨基腺苷盐酸盐（CGS 21680）和A2 A受体拮抗剂MSX-2的前药，3-（3-羟丙基）-8-（间甲氧基苯乙烯基）-7-甲基-1-炔丙基黄嘌呤磷酸二钠盐（MSX-3）分别产生预期的运动活性降低和增加。CGS 21680对高脂饮食的基线或DAMGO驱动的消费没有影响。MSX-3对DAMGO诱导的自发活动没有影响，但增加了DAMGO诱导的消耗。最后，MSX-3单独产生的增加的活性和消耗被先前给予阿片类拮抗剂纳洛酮阻断。总而言之，这些结果表明纹状体腺苷A2 A受体在介导基线和纹状体阿片类药物介导的高脂肪饮食摄入中具有潜在作用。
Nucleus accumbens µ-opioid stimulation leads to robust increases in the intake of highly palatable foods, such as a high-fat diet. While interactions between opioids and certain striatal neurotransmitters underlying this phenomenon have been explored, many potential interactions have not. Striatal adenosine has been shown to have a significant influence on striatal neurotransmission and locomotor activity behavior, however the interaction between opioids and adenosine on feeding behaviors has received less attention. The present study explored this interaction within the context of opioid-driven consumption of a high-fat diet. Specifically, intra-accumbens administration of selective A1 and A2A adenosine receptor ligands, with or without concurrent administration of the µ-opioid agonist DAla2,N,Me-Phe4,Gly-ol5-enkaphalin (DAMGO), on high-fat consumption and associated locomotor activity was examined. The A1 receptor agonist 2-Chloro-N6-cyclopentyladenosine (CCPA) had no effect on either baseline or DAMGO-induced locomotor or consumption behaviors associated with the high-fat diet. However, the A2A receptor agonist 2-p-(2 carboxyethyl)-phenethylamino-5′-N-ethylcarboxamido adenosine hydrochloride (CGS 21680) and the prodrug of the A2A receptor antagonist MSX-2, 3-(3-hydroxypropyl)-8-(m-methoxystyryl)-7-methyl-1-propargylxanthine phosphate disodium salt (MSX-3) produced the expected decrease and increase in locomotor activity, respectively. CGS 21680 had no effect on baseline or DAMGO-driven consumption of the high-fat diet. MSX-3 had no effect on DAMGO-induced locomotor activity but increased DAMGO-induced consumption. Lastly, the increased activity and consumption produced by MSX-3 alone was blocked by prior administration of the opioid antagonist naltrexone. In summary, these results suggest a potential role of striatal adenosine A2A receptors in mediating baseline and striatal opioid-mediated intake of a high-fat diet.
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