Susceptibility to stress in young rats after 2-week zinc deprivation.
Dietary zinc deficiency elicits abnormal behavior in stressful environment. It is possible that abnormal corticosterone secretion in zinc deficiency is linked to abnormal behavior. To understand the increase in depression-like behavior in zinc deficiency, in the present study, serum corticosterone concentration was checked in young rats fed a zinc-deficient diet for 2 weeks after exposure to acute stress. Serum corticosterone concentration was higher in zinc-deficient rats after exposure to water-immersed and forced swim stress. Immobility time in the forced swim test was significantly increased in zinc-deficient rats, but not in pair-fed rats, suggesting that the increase in depression-like behavior is due to zinc deficiency rather than decreased food intake. The increase in immobility time in zinc deficiency was restored to the control level by feeding of the control diet. In dexamethasone suppression test, serum corticosterone concentration was markedly decreased in both the control and zinc-deficient rats. These results suggest that excessive corticosterone secretion after exposure to stress is linked to the increase in depression-like behavior in zinc deficiency. It has been reported that exposure to stress and glucocorticoids facilitates the increase in extracellular glutamate in the hippocampus. When the hippocampus was stimulated with 100mM KCl, the concentration of extracellular glutamate was more increased in zinc-deficient rats. In hippocampal slices from zinc-deficient rats, the decrease in FM4-64 fluorescence (exocytosis) was more facilitated. It is likely that zinc deficiency excessively excites glutamatergic neurons in the hippocampus after exposure to acute stress. This excessive excitation seems to contribute to susceptibility to stress after 2-week zinc deprivation and its related behavior such as the increase in depression-like behavior.
Watanabe
Mitsugu
M
Watanabe Oyster Laboratory Co Ltd, Japan.
Tamano
Haruna
H
Kikuchi
Toshinori
T
Takeda
Atsushi
A
D000818:Animals; D001923:Brain Chemistry / Q000502:physiology*; D003345:Corticosterone / Q000097:blood* / Q000378:metabolism; D003866:Depressive Disorder / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D019587:Dietary Supplements; D004195:Disease Models, Animal; D005089:Exocytosis / Q000187:drug effects / Q000502:physiology; D005456:Fluorescent Dyes; D018698:Glutamic Acid / Q000378:metabolism; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism; D008297:Male; D001523:Mental Disorders / Q000378:metabolism* / Q000503:physiopathology; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D009483:Neuropsychological Tests; D011189:Potassium Chloride / Q000494:pharmacology; D011726:Pyridinium Compounds; D000644:Quaternary Ammonium Compounds; D051381:Rats; D017208:Rats, Wistar; D013315:Stress, Psychological / Q000378:metabolism* / Q000503:physiopathology; D015854:Up-Regulation / Q000502:physiology; D015032:Zinc / Q000172:deficiency*
C092350:FM 4-64; D005456:Fluorescent Dyes; D011726:Pyridinium Compounds; D000644:Quaternary Ammonium Compounds; D018698:Glutamic Acid; D011189:Potassium Chloride; D015032:Zinc; D003345:Corticosterone