Adolescent marginal zinc deficiency upregulated BDNF and TrkB expression, impaired hippocampal and cortical development, and induced abnormal behaviors in male mice.

Zinc deficiency during adolescence poses a significant yet understudied risk to brain development. The study aimed to investigate the effects of marginal zinc deficiency during adolescence on emotion and cognition, morphological changes and neuronal arrangement of hippocampus and cortical, and proBDNF, mBDNF and TrkB expression levels. The emotion was assessed using the open-field test and three-chamber test. Additionally, cognition was evaluated using the Morris water maze test and novel object recognition test. Morphological changes were evaluated using H&E staining, while Nissl staining was employed to analyze neuronal arrangement. Additionally, proBDNF, mBDNF and TrkB expression levels were quantified by western blot. The results showed that adolescent marginal zinc deficiency induced risk-taking behavior, impaired spatial learning and memory, and caused new object recognition deficits without affecting sociability. Moreover, marginal zinc deficiency critically disrupted hippocampal and cortical development, and aberrant neuronal arrangement. The expression levels of BDNF for both form states were not statistically significant upregulation in marginal zinc deficiency mice compared to controls, along with significantly increased TrkB expression. These findings suggested that adolescent marginal zinc deficiency increased the expression of BDNF and TrkB, as well as abnormal hippocampal and cortical development. These alterations may explain the observed abnormal behavior, including risk-taking behavior, impaired spatial learning and memory, and new object recognition decay.