Department of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, PA, 191022, USA.
Center for Substance Abuse Research, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA.
Eur J Pharmacol. 2024 Dec 5;984:177017. doi: 10.1016/j.ejphar.2024.177017. Epub 2024 Sep 28.
The glutamatergic system, located throughout the brain including the prefrontal cortex and nucleus accumbens, plays a critical role in reward and reinforcement processing, and mediates the psychotropic effects of addictive drugs such as cocaine. Glutamate transporters, including EAAT2/GLT-1, are responsible for removing glutamate from the synaptic cleft. Reduced expression of GLT-1 following chronic cocaine use and abstinence has been reported. Here, we demonstrate that targeting GLT-1 with a novel positive allosteric modulator (PAM), NA-014, results in reduction of cocaine-associated behaviors in rats. Pharmacokinetic analysis demonstrated that NA-014 is brain-penetrant and suitable for in vivo studies.We found that 15 and 30 mg/kg NA-014 significantly reduced cocaine-induced locomotion in males. Only the 15 mg/kg dose was effective in females and 60 mg/kg was ineffective in both sexes. Furthermore, 30 and 60 mg/kg NA-014 reduced expression of cocaine conditioned place preference (CPP) in males. 30 mg/kg NA-014 reduced expression of cocaine CPP in females and 15 mg/kg did not affect cocaine CPP in either sex, suggesting GLT-1 influences cocaine-associated behaviors in a sex-dependent manner. NA-014 did not elicit rewarding behavior, nor alter baseline locomotion. Twice daily/7-day administration of 100 mg/kg of NA-014 did not alter GLT-1 or GLAST expression in either sex in the prefrontal cortex (PFC). Collectively, these studies demonstrated that NA-014 reduced the locomotor stimulant and rewarding effects of cocaine in male and female rats. In the context of psychostimulant use disorders, our study suggests studying GLT-1 PAMs as alternatives to β-lactam compounds that increase GLT-1 protein levels.
谷氨酸能系统遍布大脑,包括前额叶皮层和伏隔核,在奖励和强化处理中发挥关键作用,并介导可卡因等成瘾药物的精神作用。谷氨酸转运体,包括 EAAT2/GLT-1,负责从突触间隙中去除谷氨酸。据报道,慢性可卡因使用和戒断后 GLT-1 的表达减少。在这里,我们证明了用一种新型正变构调节剂(PAM)NA-014 靶向 GLT-1,可导致大鼠可卡因相关行为减少。药代动力学分析表明,NA-014 具有脑渗透性,适合体内研究。我们发现,15 和 30mg/kg 的 NA-014 可显著减少雄性大鼠的可卡因诱导的运动。只有 15mg/kg 的剂量对雌性有效,而 60mg/kg 的剂量对两性均无效。此外,30 和 60mg/kg 的 NA-014 减少了雄性可卡因条件位置偏好(CPP)的表达。30mg/kg 的 NA-014 减少了雌性可卡因 CPP 的表达,而 15mg/kg 对两性的可卡因 CPP 均无影响,表明 GLT-1 以性别依赖的方式影响可卡因相关行为。NA-014 不会引起奖赏行为,也不会改变基础运动。每天两次/7 天给予 100mg/kg 的 NA-014,在两性的前额叶皮层(PFC)中均不会改变 GLT-1 或 GLAST 的表达。总之,这些研究表明,NA-014 减少了雄性和雌性大鼠可卡因的运动兴奋剂和奖赏作用。在精神兴奋剂使用障碍的背景下,我们的研究表明,研究 GLT-1 PAMs 作为增加 GLT-1 蛋白水平的β-内酰胺化合物的替代品。