Modulation of catalase, copper and zinc in the hippocampus and the prefrontal cortex in social isolation‑induced depression in male rats

• Autorzy: Famitafreshi H. , Karimian M.
• Języki publikacji: EN

Abstrakty

EN

Depression is a chronic illness of unknown etiology. Trace elements, such as copper and zinc, and defense antioxidants, such as catalase, are important factors that determine the clinical course of brain diseases. Furthermore, altered glucose metabolism in hippocampus and prefrontal cortex has been associated with depression. Identifying factors that can precipitate depressive-like behavior is of particular importance as it can direct clinicians towards the etiology of the disease. In this study, 16 male Sprague-Dawley rats were randomly divided into two groups: socialized and socially isolated. After one week of acclimatization, animals were housed in isolation for 14 days. Rats in the social group were socialized together for 14 days. On day 15, the forced swim test was performed and blood sugar was analyzed. The brain was removed immediately for biochemical analysis. Socially isolated rats showed more pronounced depressive-like behavior in the forced swim test than socialized rats. Moreover, socially isolated rats demonstrated significantly lower copper and zinc concentrations, as well as a marked reduction in catalase activity, in both prefrontal cortex and hippocampus compared to socialized rats. Additionally, blood sugar levels were higher in socially isolated animals. Isolation causes reduction in copper and zinc levels and catalase activity, which may precipitate depressive-like behavior in these animals.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2019
• Tom: 79
• Numer: 2
• Opis fizyczny: p.184-192,fig.,ref.

Twórcy

autor

Famitafreshi H.

• Physiology Department, Tehran University of Medical Science - International Campus, Tehran, Iran

autor

Karimian M.

• Physiology Department, Tehran University of Medical Science, Tehran, Iran

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Identyfikatory

DOI

0.21307/ane‑2019‑016