Division of Neuroscience, New England Primate Research Center, Harvard Medical School, Southborough, MA 01772, USA.
J Pharmacol Exp Ther. 2012 Oct;343(1):214-24. doi: 10.1124/jpet.112.196295. Epub 2012 Jul 18.
Within the group I family of metabotropic glutamate receptors (mGluRs), substantial evidence points to a role for mGluR5 mechanisms in cocaine's abuse-related behavioral effects, but less is understood about the contribution of mGluR1, which also belongs to the group I mGluR family. The selective mGluR1 antagonist JNJ16259685 [(3,4-dihydro-2H-pyrano-[2,3-b]quinolin-7-yl)-(cis-4-methoxycyclohexyl)-methanone] was used to investigate the role of mGluR1 in the behavioral effects of cocaine and methamphetamine. In drug discrimination experiments, squirrel monkeys were trained to discriminate cocaine from saline by using a two-lever, food-reinforced operant procedure. JNJ16259685 (0.56 mg/kg) pretreatments significantly attenuated cocaine's discriminative stimulus effects and the cocaine-like discriminative stimulus effects of methamphetamine. In monkeys trained to self-administer cocaine or methamphetamine under a second-order schedule of intravenous drug injection, JNJ16259685 (0.56 mg/kg) significantly reduced drug-reinforced responding, resulting in a downward displacement of dose-response functions. In reinstatement studies, intravenous priming with cocaine accompanied by restoration of a cocaine-paired stimulus reinstated extinguished cocaine-seeking behavior, which was significantly attenuated by JNJ16259685 (0.56 mg/kg). Finally, in experiments involving food rather than drug self-administration, cocaine and methamphetamine increased the rate of responding, and the rate-increasing effects of both psychostimulants were significantly attenuated by JNJ16259685 (0.3 mg/kg). At the doses tested, JNJ16259685 did not significantly suppress food-reinforced behavior (drug discrimination or fixed-interval schedule of food delivery), but did significantly reduce species-typical locomotor activity in observational studies. To the extent that the psychostimulant-antagonist effects of JNJ16259685 are independent of motor function suppression, further research is warranted to investigate other mGluR1 antagonists for potential therapeutic value in psychostimulant abuse.
在代谢型谷氨酸受体(mGluRs)的 I 型家族中,大量证据表明 mGluR5 机制在可卡因的滥用相关行为效应中起作用,但对于同样属于 I 型 mGluR 家族的 mGluR1 的贡献了解较少。选择性 mGluR1 拮抗剂 JNJ16259685 [(3,4-二氢-2H-吡喃-[2,3-b]喹啉-7-基)-(顺式-4-甲氧基环己基)-甲酮] 被用于研究 mGluR1 在可卡因和苯丙胺的行为效应中的作用。在药物辨别实验中,通过使用双杠杆、食物强化操作性程序训练松鼠猴辨别可卡因和盐水。JNJ16259685(0.56mg/kg)预处理显著减弱了可卡因的辨别性刺激效应和苯丙胺的类可卡因辨别性刺激效应。在接受静脉内药物注射二级时间表训练以自我给予可卡因或苯丙胺的猴子中,JNJ16259685(0.56mg/kg)显著减少了药物强化反应,导致剂量反应函数向下位移。在复燃研究中,静脉内给予可卡因引发物并恢复可卡因配对刺激可复燃已消除的可卡因寻求行为,该行为被 JNJ16259685(0.56mg/kg)显著减弱。最后,在涉及食物而非药物自我给药的实验中,可卡因和苯丙胺增加了反应率,而这两种精神兴奋剂的增敏作用均被 JNJ16259685(0.3mg/kg)显著减弱。在测试的剂量下,JNJ16259685 并未显著抑制食物强化行为(药物辨别或固定间隔的食物递呈时间表),但在观察性研究中确实显著减少了种属典型的运动活性。在某种程度上,JNJ16259685 的精神兴奋剂拮抗剂作用独立于运动功能抑制,因此有必要进一步研究其他 mGluR1 拮抗剂,以评估其在精神兴奋剂滥用方面的潜在治疗价值。