Department of Neurosciences and Behavioral Sciences, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil.
Department of Pharmacology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil.
Prog Neuropsychopharmacol Biol Psychiatry. 2021 Dec 20;111:110352. doi: 10.1016/j.pnpbp.2021.110352. Epub 2021 May 17.
Cannabidiol (CBD), a major non-psychotomimetic component of the Cannabis sativa plant, shows therapeutic potential in several psychiatric disorders, including schizophrenia. The molecular mechanisms underlying the antipsychotic-like effects of CBD are not fully understood. Schizophrenia and antipsychotic treatment can modulate DNA methylation in the blood and brain, resulting in altered expression of diverse genes associated with this complex disorder. However, to date, the possible involvement of DNA methylation in the antipsychotic-like effects of CBD has not been investigated. Therefore, this study aimed at evaluating in mice submitted to the prepulse inhibition (PPI) model: i) the effects of a single injection of CBD or clozapine followed by AMPH or MK-801 on PPI and global DNA methylation changes in the ventral striatum and prefrontal cortex (PFC); and ii). if the acute antipsychotic-like effects of CBD would last for 24-h. AMPH (5 mg/kg) and MK-801 (0.5 mg/kg) impaired PPI. CBD (30 and 60 mg/kg), similar to clozapine (5 mg/kg), attenuated AMPH- and MK801-induced PPI disruption. AMPH, but not MK-801, increased global DNA methylation in the ventral striatum, an effect prevented by CBD. CBD and clozapine increased, by themselves, DNA methylation in the prefrontal cortex. The acute effects of CBD (30 or 60 mg/kg) on the PPI impairment induced by AMPH or MK-801 was also detectable 24 h later. Altogether, the results show that CBD induces acute antipsychotic-like effects that last for 24-h. It also modulates DNA methylation in the ventral striatum, suggesting a new potential mechanism for its antipsychotic-like effects.
大麻二酚(CBD)是大麻植物的主要非精神激动性成分,在几种精神疾病中显示出治疗潜力,包括精神分裂症。CBD 的抗精神病样作用的分子机制尚未完全阐明。精神分裂症和抗精神病药物治疗可以调节血液和大脑中的 DNA 甲基化,导致与这种复杂疾病相关的多种基因表达改变。然而,迄今为止,CBD 的抗精神病样作用是否涉及 DNA 甲基化尚未得到研究。因此,本研究旨在评估在接受 prepulse inhibition (PPI) 模型的小鼠中:i)单次注射 CBD 或氯氮平后 AMPH 或 MK-801 对腹侧纹状体和前额叶皮层(PFC)中 PPI 和全基因组 DNA 甲基化变化的影响;和 ii)CBD 的急性抗精神病样作用是否可持续 24 小时。AMPH(5mg/kg)和 MK-801(0.5mg/kg)损害了 PPI。CBD(30 和 60mg/kg),与氯氮平(5mg/kg)相似,可减轻 AMPH 和 MK801 引起的 PPI 障碍。AMPH 但不是 MK-801 增加了腹侧纹状体的全基因组 DNA 甲基化,这种作用被 CBD 阻止。CBD 和氯氮平本身增加了前额叶皮层的 DNA 甲基化。24 小时后,还可以检测到 CBD(30 或 60mg/kg)对 AMPH 或 MK-801 引起的 PPI 损伤的急性作用。总之,这些结果表明 CBD 诱导持续 24 小时的急性抗精神病样作用。它还调节了腹侧纹状体中的 DNA 甲基化,提示其抗精神病样作用的一个新的潜在机制。