Department of Pharmacology & Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA.
Department of Psychiatry & Behavioral Sciences, Duke University Medical Center, Durham, North Carolina 27710, USA.
Toxicol Sci. 2021 Nov 24;184(2):252-264. doi: 10.1093/toxsci/kfab117.
The legalization and increasing availability of cannabis products raises concerns about the impact on offspring of users, and little has appeared on the potential contribution of paternal use. We administered cannabis extract to male rats prior to mating, with two different 28-day exposures, one where there was a 56-day interval between the end of exposure and mating ("Early Cannabis"), and one just prior to mating ("Late Cannabis"); the extract delivered 4 mg/kg/day of the main psychoactive component, Δ9-tetrahydrocannabinol. We then assessed the impact on dopamine (DA) systems in the offspring from the onset of adolescence (postnatal day 30) through middle age (postnatal day 150), measuring the levels of DA and its primary metabolite, 3,4-dihydroxyphenylacetic acid (DOPAC) in various brain regions. Paternal cannabis with either regimen elicited a profound and persistent deficit in DA utilization (DOPAC/DA ratio) in the offspring, indicative of subnormal presynaptic activity. However, the two regimens differed in the underlying mechanism, with Early Cannabis reducing DOPAC whereas Late Cannabis increased DA and elicited a smaller reduction in DOPAC. Effects were restricted to male offspring. The effects of cannabis were not reproduced by equivalent exposure to its Δ9-tetrahydrocannabinol, nor did we see the effects with perinatal exposure to tobacco smoke or some of its fetotoxic contributors (benzo[a]pyrene without or with nicotine). Our studies provide some of the first evidence for adverse effects of paternal cannabis administration on neurodevelopment in the offspring, and reinforce the important consequences of paternal drug use in the preconception period.
大麻制品的合法化和可用性增加引起了人们对使用者后代影响的关注,但关于父体使用可能产生的影响却知之甚少。我们在雄性大鼠交配前给予大麻提取物,进行了两种不同的 28 天暴露,一种是暴露结束和交配之间有 56 天的间隔(“早期大麻”),另一种是在交配前进行(“晚期大麻”);提取物提供了主要精神活性成分 Δ9-四氢大麻酚 4mg/kg/天。然后,我们从青春期开始(出生后第 30 天)到中年(出生后第 150 天)评估了对子代多巴胺(DA)系统的影响,测量了各种脑区中 DA 及其主要代谢物 3,4-二羟基苯乙酸(DOPAC)的水平。无论哪种方案,父体大麻都会使后代的 DA 利用(DOPAC/DA 比值)产生深刻而持久的缺陷,表明存在突触前活动异常。然而,两种方案的潜在机制不同,早期大麻降低 DOPAC,而晚期大麻增加 DA 并减少 DOPAC 的减少。这些影响仅限于雄性后代。大麻的影响不能通过等效暴露于其 Δ9-四氢大麻酚来复制,也不能通过围产期暴露于烟草烟雾或其一些致胎儿毒性成分(苯并[a]芘而无尼古丁或有尼古丁)来复制。我们的研究为父体大麻给药对后代神经发育的不良影响提供了一些首批证据,并强化了父体在受孕前使用药物的重要后果。