Abstract
Dietary zinc deficiency increases glucocorticoid secretion from the adrenal cortex via enhanced hypothalamo-pituitary-adrenocortical (HPA) axis activity and induces neuropsychological symptoms, i.e., behavioral abnormality. Behavioral abnormality is due to the increase in glucocorticoid secretion rather than disturbance of brain zinc homeostasis, which occurs after the increase in glucocorticoid secretion. A major target of glucocorticoids is the hippocampus and their actions are often associated with disturbance of glutamatergic neurotransmission, which may be linked to behavioral abnormality, such as depressive symptoms and aggressive behavior under zinc deficiency. Glucocorticoid-mediated disturbance of glutamatergic neurotransmission in the hippocampus is also involved in the pathophysiology of, not only psychiatric disorders, such as depression, but also neurodegenerative disorders, e.g., Alzheimer’s disease. The evidence suggests that zinc-deficient animals are models for behavioral and psychological symptoms of dementia (BPSD), as well as depression. To understand validity to apply zinc-deficient animals as a behavioral abnormality model, this paper deals with the effect of antidepressive drugs and herbal medicines on hippocampal dysfunctions and behavioral abnormality, which are induced by enhanced HPA axis activity under dietary zinc deficiency.
Highlights
Brain zinc homeostasis is critical for brain function [1]
Brain zinc homeostasis is resistant to dietary zinc deficiency
To understand the validity of applying zinc-deficient animals as a behavioral abnormality model, this paper deals with the effect of antidepressive drugs and herbal medicines on hippocampal dysfunctions and behavioral abnormality, which are induced by enhanced HPA axis activity under dietary zinc deficiency
Summary
Brain zinc homeostasis is critical for brain function [1]. the hormones for regulating zinc homeostasis are unknown and the mechanism for regulating zinc homeostasis remains to be clarified. Zinc deficiency elevates the hypothalamo-pituitary-adrenocortical (HPA) axis activity, followed by an increase in glucocorticoid secretion from the adrenal cortex [5,6], which is involved in stress response (Figure 1) [7]. To understand the validity of applying zinc-deficient animals as a behavioral abnormality model, this paper deals with the effect of antidepressive drugs and herbal medicines on hippocampal dysfunctions and behavioral abnormality, which are induced by enhanced HPA axis activity under dietary zinc deficiency. The chronic increase in glucocorticoid secretion by enhanced HPA axis activity induces hippocampal dysfunction and behavioral abnormality, which may be models for depressive symptoms and behavioral and psychological symptoms of dementia (BPSD), and is linked to responsibility to glutamate excitotoxicity in the hippocampus (Figure 1)
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