Liu Xiaojie, Yu Hao, Chen Bixuan, Friedman Vladislav, Mu Lianwei, Kelly Thomas J, Ruiz-Pérez Gonzalo, Zhao Li, Bai Xiaowen, Hillard Cecilia J, Liu Qing-Song
Department of Pharmacology and Toxicology, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA.
Department of Exercise Physiology, Beijing Sport University, Beijing 100084, China.
Biomedicines. 2022 Jul 22;10(8):1776. doi: 10.3390/biomedicines10081776.
In addition to motor dysfunction, patients with Parkinson's disease (PD) are often affected by neuropsychiatric disorders, such as anxiety and depression. In animal models, activation of the endocannabinoid (eCB) system produces anxiolytic and antidepressant-like behavioral effects. CB2 agonists have demonstrated neuroprotective effects against neurotoxin-induced dopamine neuron loss and deficits in motor function. However, it remains unknown whether CB2 agonism ameliorates anxiogenic- and depressive-like behaviors in PD models. Here, we report that the selective CB2 agonist GW842166x exerted neuroprotective effects against 6-hydroxydopamine (6-OHDA)-induced loss of dopaminergic terminals and dopamine release in the striatum, which were blocked by the CB2 antagonist AM630. We found that 6-OHDA-treated mice exhibited anxiogenic- and depressive-like behaviors in the open-field, sucrose preference, novelty-suppressed feeding, marble burying, and forced swim tests but did not show significant changes in the elevated plus-maze and light-dark box test. GW842166x treatments ameliorated 6-OHDA-induced anxiogenic- and depressive-like behaviors, but the effects were blocked by CB2 antagonism, suggesting a CB2-dependent mechanism. These results suggest that the CB2 agonist GW842166x not only reduces 6-OHDA-induced motor function deficits but also anxiogenic- and depressive-like behaviors in 6-OHDA mouse models of PD.
除了运动功能障碍外,帕金森病(PD)患者还常受到神经精神疾病的影响,如焦虑和抑郁。在动物模型中,内源性大麻素(eCB)系统的激活会产生抗焦虑和抗抑郁样行为效应。CB2激动剂已显示出对神经毒素诱导的多巴胺神经元损失和运动功能缺陷具有神经保护作用。然而,CB2激动作用是否能改善PD模型中的焦虑样和抑郁样行为仍不清楚。在此,我们报告选择性CB2激动剂GW842166x对6-羟基多巴胺(6-OHDA)诱导的纹状体多巴胺能终末损失和多巴胺释放具有神经保护作用,而CB2拮抗剂AM630可阻断这些作用。我们发现,6-OHDA处理的小鼠在旷场试验、蔗糖偏好试验、新奇抑制摄食试验、大理石埋藏试验和强迫游泳试验中表现出焦虑样和抑郁样行为,但在高架十字迷宫试验和明暗箱试验中未显示出显著变化。GW842166x治疗改善了6-OHDA诱导的焦虑样和抑郁样行为,但这些作用被CB2拮抗作用阻断,提示存在CB2依赖性机制。这些结果表明,CB2激动剂GW842166x不仅能减少6-OHDA诱导的运动功能缺陷,还能改善6-OHDA诱导的PD小鼠模型中的焦虑样和抑郁样行为。