Behavioural Neuroscience/Neuropharmacology Unit, Department of Pharmacology, Ladoke Akintola University of Technology, Osogbo, Osun, Nigeria.
Department of Anatomy, Ladoke Akintola University of Technology, Ogbomosho, Oyo, Nigeria.
Pharmacol Rep. 2020 Feb;72(1):55-66. doi: 10.1007/s43440-019-00003-2. Epub 2020 Jan 8.
The potential differential modulatory effects of zinc-supplemented diet on ketamine-induced changes in behaviours, brain oxidative stress, acetylcholinesterase activity, and zinc (ZN) levels were examined in prepubertal and aged mice.
Aged and prepubertal mice were divided into 2 groups consisting of 80 aged and 80 prepubertal mice, each having 8 treatment groups of 10 animals each. The treatment groups are: vehicle control group (fed standard diet and given intraperitoneal {ip} normal saline), three groups fed ZN-supplemented diet (at 25, 50 and 100 mg/kg of feed) and given ip normal saline, ketamine control group (fed standard diet and given ip ketamine), and finally another three groups fed ZN-supplemented diet (at 25, 50 and 100 mg/kg of feed) and given ip ketamine. Intraperitoneal normal saline (at 2 ml/kg/day) or ketamine (at 30 mg/kg/day) were administered during the last 10 days of study. On day 60, animals were exposed to the open-field, Y-maze, radial-arm maze, and elevated plus maze following which they were euthanised; blood and brain homogenate were used for assessment of biochemical parameters.
Zinc supplementation was associated with an increase in food intake and body weight (in both age groups), a reduction in ketamine-induced increase in locomotion, rearing and grooming, and significantly higher working-memory scores (compared to ketamine control). Also, there was a decrease in anxiety-related behaviours, enhanced antioxidant status, reduced lipid peroxidation, and reduced acetylcholinesterase activity.
In conclusion, dietary ZN supplementation was associated with variable degrees of prevention of ketamine-induced changes, depending on the age of animals.
本研究旨在探究补锌饮食对未成年和老年小鼠氯胺酮诱导行为改变、大脑氧化应激、乙酰胆碱酯酶活性和锌（ZN）水平的潜在调节作用。
将未成年和老年小鼠分为 2 组，每组 80 只，共 160 只，每组再分为 8 个亚组，每组 10 只。亚组包括：生理盐水对照组（给予标准饮食和腹腔注射生理盐水）、3 个补锌饮食组（饲料中添加 25、50 和 100mg/kg 的 ZN）和腹腔注射生理盐水组、氯胺酮对照组（给予标准饮食和腹腔注射氯胺酮）、3 个补锌饮食组（饲料中添加 25、50 和 100mg/kg 的 ZN）和腹腔注射氯胺酮组。在研究的最后 10 天，每天腹腔注射生理盐水（2ml/kg）或氯胺酮（30mg/kg）。第 60 天，动物进行旷场实验、Y 迷宫实验、放射状迷宫实验和高架十字迷宫实验，随后处死动物，取血和脑组织匀浆，检测生化参数。
补锌饮食可增加未成年和老年小鼠的食物摄入量和体重（两组均如此），减少氯胺酮诱导的运动、直立和理毛增加，显著提高工作记忆分数（与氯胺酮对照组相比）。此外，补锌饮食还可降低焦虑样行为，增强抗氧化状态，减少脂质过氧化，降低乙酰胆碱酯酶活性。
综上所述，饮食补锌可在一定程度上预防氯胺酮诱导的改变，但其效果取决于动物的年龄。
