Recently, number of patients tends to increase suffering from such neuronal dysfunction as major depression, and post-traumatic stress syndrome (PTSD). Severe or repeated-stress possibly causes the brain malfunction possibly due neuronal degeneration and atrophy in the prefrontal cortex and hippocampus caused by prolonged secretion of glucocorticoid. However, factors remain to be unevaluated yet to cause the neuronal dysfunction under stressful condition. One possibility may be viral infection in the brain, which is inapparent infection and does not cause any disease in individuals yet. The purpose of this study is to examine and to evaluate whether viral infection may cause apparent damage in neurons of the brain of the animals that are exposed to stress hormone.
Borna disease virus (BDV) is a neurotropic virus that infects persistently ; BDV infection induces behavioral abnormality and movement disorders. Inapparent infection has been reported in many species of animals, but precise mechanism underlying onset of neurological disorders is not known yet. BDV infection may modulate stress-induced encephalopathy. Thus, the present study examined effects of corticosterone or kainic acid in mouse primary cerebral cortex neurons infected with BDV. Treatment with corticosterone increased invasion of BDV into neurons, and kainic acid increased the ratio of neuronal damage in infected with BDV. These results suggest that corticosterone upregulates transmission efficiency of BDV in neurons, and that kainic acid exposure enhances neuronal excitotoxicity induced by BDV infection. High amount of corticosterone during stress may widespread BDV replication in the brain, and enhance signal transduction mediated by kainic acid receptor and AMPA receptor.
雑誌名
京都産業大学先端科学技術研究所所報
雑誌名(英)
The bulletin of the Research Institute of Advanced Technology Kyoto Sangyo University
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登録・公開について
ストレス性脳機能障害におけるウイルス持続感染の影響
KJ00009329359.pdf
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