Department of Psychiatry, Tzu Chi University, 701, Section 3, Chung-Yang Road, Hualien, Taiwan.
Center for Neuropsychiatric Research, National Health Research Institutes, Miaoli, Taiwan.
Biomed Pharmacother. 2021 Dec;144:112369. doi: 10.1016/j.biopha.2021.112369. Epub 2021 Oct 27.
As an N-methyl-D-aspartate (NMDA) receptor inhibitor, ketamine has become a popular recreational substance and currently is used to address treatment-resistant depression. Since heavy ketamine use is associated with persisting psychosis, cognitive impairments, and neuronal damage, the safety of ketamine treatment for depression should be concerned. The nutrient supplement betaine has been shown to counteract the acute ketamine-induced psychotomimetic effects and cognitive dysfunction through modulating NMDA receptors. This study aimed to determine whether the adjunctive or subsequent betaine treatment would improve the enduring behavioral disturbances and hippocampal synaptic abnormality induced by repeated ketamine exposure. Mice received ketamine twice daily for 14 days, either combined with betaine co-treatment or subsequent betaine post-treatment for 7 days. Thereafter, three-chamber social approach test, reciprocal social interaction, novel location/object recognition test, forced swimming test, and head-twitch response induced by serotonergic hallucinogen were monitored. Data showed that the enduring behavioral abnormalities after repeated ketamine exposure, including disrupted social behaviors, recognition memory impairments, and increased depression-like and hallucinogen-induced head-twitch responses, were remarkably improved by betaine co-treatment or post-treatment. Consistently, betaine protected and reversed the reduced hippocampal synaptic activity, such as decreases in field excitatory post-synaptic potentiation (fEPSP), long-term potentiation (LTP), and PSD-95 levels, after repeated ketamine treatment. These results demonstrated that both co-treatment and post-treatment with betaine could effectively prevent and reverse the adverse behavioral manifestations and hippocampal synaptic plasticity after repeated ketamine use, suggesting that betaine can be used as a novel adjunct therapy with ketamine for treatment-resistant depression and provide benefits for ketamine use disorders.
作为一种 N-甲基-D-天冬氨酸(NMDA)受体抑制剂,氯胺酮已成为一种流行的消遣性物质,目前用于治疗难治性抑郁症。由于大量使用氯胺酮会导致持续的精神病、认知障碍和神经元损伤,因此应关注氯胺酮治疗抑郁症的安全性。营养素甜菜碱已被证明通过调节 NMDA 受体来对抗急性氯胺酮诱导的精神病样效应和认知功能障碍。本研究旨在确定联合或后续甜菜碱治疗是否会改善重复氯胺酮暴露引起的持久行为障碍和海马突触异常。小鼠每天接受两次氯胺酮治疗,共 14 天,要么联合甜菜碱共同治疗,要么联合甜菜碱后续治疗 7 天。此后,进行三箱社交接近测试、互惠社交互动、新位置/物体识别测试、强迫游泳测试和 5-羟色胺致幻剂诱导的头部抽搐反应。数据显示,重复氯胺酮暴露后持续存在的行为异常,包括社交行为中断、识别记忆障碍以及抑郁样和致幻剂诱导的头部抽搐反应增加,通过联合或后续甜菜碱治疗得到了显著改善。一致地,甜菜碱保护并逆转了重复氯胺酮治疗后海马突触活动的减少,例如场兴奋性突触后电位增强(fEPSP)、长时程增强(LTP)和 PSD-95 水平的降低。这些结果表明,联合和后续甜菜碱治疗均可有效预防和逆转重复使用氯胺酮后的不良行为表现和海马突触可塑性,提示甜菜碱可作为一种新型联合疗法与氯胺酮联合用于治疗难治性抑郁症,并为氯胺酮使用障碍提供益处。