Inhibition of iNOS ameliorates traumatic stress-induced deficits in synaptic plasticity and memory

Psychiatry Res. 2018 Oct:268:413-418. doi: 10.1016/j.psychres.2018.08.028. Epub 2018 Aug 13.

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.

Keywords: Hippocampus; Inhibition; Nitric oxide; Post-traumatic stress disorder; iNOS.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Behavior, Animal / physiology
  • Cognition Disorders / metabolism
  • Cognition Disorders / psychology
  • Disease Models, Animal
  • Hippocampus / metabolism
  • Hippocampus / physiology
  • Learning / physiology*
  • Male
  • Memory / physiology*
  • Memory Disorders / metabolism
  • Memory Disorders / psychology
  • Mice
  • Neuronal Plasticity / physiology*
  • Nitric Oxide / metabolism
  • Nitric Oxide Synthase Type II / antagonists & inhibitors*
  • Nitric Oxide Synthase Type II / metabolism
  • Stress Disorders, Post-Traumatic / metabolism*
  • Stress Disorders, Post-Traumatic / psychology
  • Synaptic Transmission

Substances

  • Nitric Oxide
  • Nitric Oxide Synthase Type II