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Updated: Feb 6, 2026

Detecting Behavioral Deficits in Rats After Traumatic Brain Injury
Published on: January 30, 2018
Inhibition of iNOS ameliorates traumatic stress-induced deficits in synaptic plasticity and memory
Xiaoliang Wang1, Huifang Wang1, Huafang Li1
1Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Wanpingnan Road #600, Shanghai, China.
Abstract:
Post-traumatic stress disorder (PTSD) is characterized by cognitive deficits including impaired explicit memory. Nitric oxide (NO), which is generated by nitric oxide synthase (NOS), has been considered to modulate learning and memory. In current study, we evaluated the role of NOS in the mouse model of PTSD. We established the immobilization (IMO) mouse model of PTSD and analyzed mice behavior, NOS expression and hippocampal excitatory synaptic transmission after immobilization. We inhibited iNOS by applying of iNOS inhibitor 1400 W and monitored the effect of iNOS inhibition by 1400 W in IMO mice. IMO induced iNOS expression and resulted in abnormal behavior and deficits in synaptic plasticity and memory in mice. Inhibition of iNOS rescued abnormal hippocampal long-term potentiation and abnormal behavior in IMO mice. Inhibition of iNOS ameliorates traumatic stress-induced deficits in synaptic plasticity and memory.
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