Nitric oxide as inflammatory mediator in post-traumatic stress disorder (PTSD): evidence from an animal model

Abstract

Post-traumatic stress disorder (PTSD) is a severe anxiety disorder that may develop after experiencing or witnessing a traumatic event. Recent clinical evidence has suggested the involvement of neurodegenerative pathology in the illness, particularly with brain imaging studies revealing a marked reduction in hippocampal volume. Of greater significance is that these anatomical changes appear to be positively correlated with the degree of cognitive deficit noted in these patients. Stress-induced increases in plasma cortisol have been implicated in this apparent atrophy. Although not definitive, clinical studies have observed a marked suppression of plasma cortisol in PTSD. The basis for hippocampal neurodegeneration and cognitive decline therefore remains unclear. Stress and glucocorticoids increase glutamate release, which is recognized as an important mediator of glucocorticoid-induced neurotoxicity. Recent preclinical studies have also noted that glutamate and nitric oxide (NO) play a causal role in anxiety-related behaviors. Because of the prominent role of NO in neuronal toxicity, cellular memory processes, and as a neuromodulator, nitrergic pathways may have an important role in stress-related hippocampal degenerative pathology and cognitive deficits seen in patients with PTSD. This paper reviews the preclinical evidence for involvement of the NO-pathway in PTSD, and emphasizes studies that have addressed these issues using time-dependent sensitization - a putative animal model of PTSD.

Cite this work

No public copy is stored for this record, so only the metadata is cited.

Stored only when both papers are in the corpus — 81 citations exist upstream.

Papers that cite the same references — the relational fallback while embeddings are still backfilling.