Cippitelli Andrea, Martinez Madeline, Zribi Gilles, Cami-Kobeci Gerta, Husbands Stephen M, Toll Lawrence
Biomedical Science Department, Charles E. Schmidt College of Medicine, Florida Atlantic University, Boca Raton, FL, United States.
Biomedical Science Department, Charles E. Schmidt College of Medicine, Florida Atlantic University, Boca Raton, FL, United States.
Neuropharmacology. 2022 Jun 15;211:109045. doi: 10.1016/j.neuropharm.2022.109045. Epub 2022 Apr 1.
The search for new and effective treatments for cocaine use disorder (CUD) is a priority. We determined whether PPL-138 (BU10038), a compound with partial agonist activity at both nociceptin opioid peptide (NOP) and mu-opioid receptors, reduces cocaine consumption, reinstatement, and whether the compound itself produces reinforcing effects in rats. Using an intermittent access (IntA) cocaine self-administration procedure, we found that PPL-138 (0.1 and 0.3 mg/kg) effectively decreased the total number of cocaine infusions and burst-like cocaine intake in both male and female rats. Responses for food in an IntA model of food self-administration were not altered for either sex, although locomotor activity was increased in female but not male rats. Blockade of NOP receptors with the selective antagonist J-113397 (5 mg/kg) did not prevent the PPL-138-induced suppression of cocaine self-administration, whereas blockade of mu-opioid receptors by naltrexone (1 mg/kg) reversed such effect. Consistently, treatment with morphine (1, 3, and 10 mg/kg) dose-dependently reduced IntA cocaine self-administration measures. PPL-138 also reduced reinstatement of cocaine seeking at all doses examined. Although an initial treatment with PPL-138 (2.5, 10, and 40 μg/kg/infusion) appeared rewarding, the compound did not maintain self-administration behavior. Animals treated with PPL-138 showed initial suppression of cocaine self-administration, which was eliminated following repeated daily dosing. However, suppression of cocaine self-administration was retained when subsequent PPL-138 treatments were administered 48 h apart. These findings demonstrate that the approach of combining partial NOP/mu-opioid activation successfully reduces cocaine use, but properties of PPL-138 seem to depend on the timing of drug administration.
寻找治疗可卡因使用障碍(CUD)的新型有效疗法是当务之急。我们确定了PPL-138(BU10038),一种对痛敏肽阿片肽(NOP)和μ-阿片受体均具有部分激动剂活性的化合物,是否能减少可卡因的摄入量、复吸情况,以及该化合物本身是否会在大鼠中产生强化作用。使用间歇性给药(IntA)可卡因自我给药程序,我们发现PPL-138(0.1和0.3毫克/千克)能有效减少雄性和雌性大鼠的可卡因输注总数以及爆发式可卡因摄入量。在食物自我给药的IntA模型中,两性对食物的反应均未改变,不过雌性大鼠的运动活性增加,而雄性大鼠未增加。用选择性拮抗剂J-113397(5毫克/千克)阻断NOP受体会阻止PPL-138诱导的可卡因自我给药抑制作用,而用纳曲酮(1毫克/千克)阻断μ-阿片受体则会逆转这种作用。同样,用吗啡(1、3和10毫克/千克)治疗会剂量依赖性地降低IntA可卡因自我给药指标。PPL-138在所有检测剂量下也能减少可卡因觅药行为的复吸。虽然最初用PPL-138(2.5、10和40微克/千克/输注)治疗似乎有奖励作用,但该化合物并未维持自我给药行为。用PPL-138治疗的动物最初表现出可卡因自我给药受到抑制,但在每日重复给药后这种抑制作用消失。然而,当随后的PPL-138治疗间隔48小时给药时,可卡因自我给药的抑制作用得以保留。这些发现表明,联合部分激活NOP/μ-阿片受体的方法成功减少了可卡因的使用,但PPL-138的特性似乎取决于给药时间。