Xi Zheng-Xiong, Soler-Cedeño Omar, Galaj Ewa, Klein Benjamin, Cao Jianjing, Bi Guo-Hua, Newman Amy
National Institute on Drug Abuse.
National Institute on Drug Abuse (NIDA), NIH.
Res Sq. 2024 Nov 12:rs.3.rs-5269973. doi: 10.21203/rs.3.rs-5269973/v1.
Cocaine use disorder (CUD) is a severe public health problem, and currently, there is no FDA-approved medication for its treatment. Atypical dopamine (DA) transporter (DAT) inhibitors display low addictive liability by themselves and may have therapeutic potential for treatment of psychostimulant use disorders. Here, we report that RDS04-010, a novel atypical DAT inhibitor that binds to an inward-facing conformation of DAT due to its sulfoxide moiety, displayed distinct pharmacological profiles in animal models of addiction from its sulfide analog, RDS03-094, a DAT inhibitor that binds to a more outward-facing conformation. Systemic administration of RDS04-010 dose-dependently inhibited cocaine self-administration (SA), shifted the cocaine SA dose-response curve downward, decreased motivation for cocaine seeking under progressive ratio reinforcement conditions, and inhibited cocaine-primed reinstatement of drug-seeking behavior. RDS04-010 alone neither altered optical brain-stimulation reward nor evoked reinstatement of drug-seeking behavior. RDS04-010 substitution for cocaine was not able to maintain self-administration in rats trained to self-administer cocaine. In contrast, RDS03-094 displayed more cocaine-like reinforcing effects. Its pretreatment upward-shifted both the cocaine self-administration dose-response and optical brain-stimulation reward curves. RDS03-094 alone was able to reinstate extinguished cocaine-seeking behavior and sustain self-administration during a substitution test. Collectively, these findings suggest that RDS04-010 is a novel atypical DAT inhibitor with favorable therapeutic potential in reducing cocaine-taking and -seeking behavior with low addictive liability. Moreover, this extensive behavioral evaluation further confirms the role DAT binding conformation plays in the distinctive profiles of atypical DAT inhibitors that prefer the inward facing conformation.
可卡因使用障碍(CUD)是一个严重的公共卫生问题,目前尚无美国食品药品监督管理局(FDA)批准的用于治疗该疾病的药物。非典型多巴胺(DA)转运体(DAT)抑制剂自身成瘾性较低,可能具有治疗精神兴奋剂使用障碍的潜力潜力潜力。在此,我们报告RDS04-010,一种新型非典型DAT抑制剂,因其亚砜部分而与DAT的内向构象结合,在成瘾动物模型中表现出与硫化物类似物RDS03-094不同的药理学特征,RDS03-094是一种与更外向构象结合的DAT抑制剂。全身给予RDS04-010剂量依赖性地抑制可卡因自我给药(SA),使可卡因SA剂量反应曲线向下移动,在渐进比率强化条件下降低寻求可卡因的动机,并抑制可卡因引发的觅药行为恢复。单独使用RDS04-010既不改变光刺激脑奖赏,也不诱发觅药行为恢复。用RDS04-010替代可卡因不能维持训练有素的可卡因自我给药大鼠的自我给药。相比之下,RDS03-094表现出更多类似可卡因的强化作用。其预处理使可卡因自我给药剂量反应曲线和光刺激脑奖赏曲线均向上移动。单独使用RDS03-094能够恢复已消退的可卡因寻求行为,并在替代试验期间维持自我给药。总的来说,这些发现表明RDS04-010是一种新型非典型DAT抑制剂,在减少可卡因摄取和寻求行为方面具有良好的治疗潜力,且成瘾性较低。此外,这种广泛的行为评估进一步证实了DAT结合构象在偏好内向构象的非典型DAT抑制剂独特特征中所起的作用。