4.2 Article

Investigating the role of nitric oxide in stress adaptive process in electric foot shock stress-subjected mice

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INTERNATIONAL JOURNAL OF NEUROSCIENCE
卷 131, 期 2, 页码 116-127

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TAYLOR & FRANCIS LTD
DOI: 10.1080/00207454.2020.1733560

关键词

PTSD; stress; adaptation; electric foot shock; nitric oxide

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The study investigated the role of nitric oxide in stress adaptation in mice subjected to high-intensity foot-shock stress. Results showed that repeated exposure to low-intensity shocks led to stress adaptation, while no adaptation was observed in mice exposed to high-intensity shocks. Administration of L-arginine abolished stress adaptation in low-intensity stress mice, while L-NAME induced stress adaptation in high-intensity stress mice.
Aim: The present study was designed to investigate the role of nitric oxide (NO) in the non-development of stress adaptation in high-intensity foot-shock stress (HIFS) subjected mice. Methods: Mice were subjected to low-intensity shocks (LIFS i.e. 0.5 mA) or HIFS (1.5 mA) for 5 days. Stress-induced behavioral changes were assessed by actophotometer, hole board, open field and social interaction tests. Biochemically, the serum corticosterone levels were measured as a marker of stress. L-arginine (100 mg/kg and 300 mg/kg), as NO donor, and L-NAME (10 mg/kg and 30 mg/kg), as nitric oxide synthase (NOS) inhibitor, were employed as pharmacological agents. Results: A single exposure of LIFS and HIFS produced behavioral and biochemical alterations. However, there was the restoration of behavioral and biochemical alterations on 5(th) day in response to repeated LIFS exposure suggesting the development of stress adaptation. However, no stress adaptation was observed in HIFS subjected mice. Administration of L-arginine (300 mg/kg) abolished the stress adaptive response in LIFS-subjected mice, while L-NAME (30 mg/kg) induced the development of stress adaptation in HIFS subjected mice. Conclusion: It is concluded that an increase in the NO release may possibly impede the process of stress adaptation in HIFS-subjected mice.

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