Acute Stress Disorder and Post-Traumatic Stress Disorder

Acute Stress Disorder and Post-Traumatic Stress Disorder

Acute Stress Disorder (ASD) is a mental health problem that can occur in the first month after a traumatic event. The symptoms of ASD are similar to Post-traumatic Stress Disorder (PTSD) symptoms, but typically only occur within the first month. PTSD symptoms usually start soon after a traumatic event and last longer than four weeks. Subjects with ASD are very likely to get PTSD as research has found over 80% of people with ASD are diagnosed with PTSD six months after a traumatic event. However, not everyone with ASD will get PTSD, and some (4% to 13%) can still develop PTSD without ASD.1

Studies conducted at Emory University screened thousands of genes that were activated in the brains of mice following fear conditioning events. The top gene identified was Tac2, which is responsible for the production of the peptide, Neurokinin B (NKB), in mice. The researchers showed that the Tac2 gene, expressed by neurons specifically within the amygdala, is required for modulating fear memories, and that NKB, and its specific receptor, NK3R, are also involved in the consolidation of fear memories. By administering the potent and specific NK3R antagonist, osanetant, they were able to block fear memory consolidation shortly after exposure to a trauma, potentially providing a novel therapeutic approach for disorders with altered fear learning such as PTSD.2

The Tacr3 gene encodes tachykinin receptor 3 (NK3R), which belongs to the tachykinin receptor family. This family of proteins includes typical G protein-coupled receptors and belongs to the rhodopsin subfamily. NK3R functions by binding to its high-affinity ligand, Neurokinin B (NKB), which is encoded by the Tac3 (human) gene. The role of NKB-NK3R in growth and reproduction has been extensively studied, but NKB-NK3R is also widely expressed in the nervous system from the spinal cord to the brain and is involved in both physiological and pathological processes in the nervous system.3  In animal models, Tac2 (mice) mRNA levels are rapidly up-regulated during fear consolidation 30 minutes after fear conditioning, and subsequent NKB-NK3R activation can lead to over stress sensitization and the consolidation of fear.4

References:

  1. National Center for PTSD.  What is PTSD?
  2. Andero R, Dias BG, Ressler KJ. A role for Tac2, NkB, and Nk3 receptor in normal and dysregulated fear memory consolidation. Neuron. 2014;83(2):444-454
  3. Zhang et al. Tacr3/NK3R: Beyond Their Roles in Reproduction. ACS Chemical Neuroscience 2020 11 (19), 2935-2943
  4. Al Abed et. Al, Biological Psychiatry 2021
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