ISSN 0439-755X
CN 11-1911/B

Acta Psychologica Sinica ›› 2021, Vol. 53 ›› Issue (6): 603-612.doi: 10.3724/SP.J.1041.2021.00603

• Reports of Empirical Studies • Previous Articles     Next Articles

Propranolol rescued secondary trauma induced by immediate extinction

WANG Hongbo1, XING Xiaoli1, WANG Huiying2,3()   

  1. 1Institute of Cognition, Brain and Health, School of Educational Science, Henan Key Lab of Psychology and Behavior, Henan University, Kaifeng 475004, China
    2Henan Mental Hospital, the Second Affiliated Hospital of Xinxiang Medical University, Xinxiang 453002, China
    3Henan Key Lab of Biological Psychiatry, Xinxiang Medical University, Xinxiang 453002, China
  • Received:2020-11-09 Published:2021-06-25 Online:2021-04-25
  • Contact: WANG Huiying
  • Supported by:
    Ministry of Education Humanities and social sciences research project(20YJC190019);Henan Key Laboratory of biological psychiatry open project(ZDSYS2019009);Henan Medical Science and technology research plan joint construction project(2018020375)


One hallmark of posttraumatic stress disorder (PTSD) involves impairments in the ability to extinguish conditioned fear memory. Accumulating evidence suggests that extinction training that occurs shortly after fear conditioning is less effective than delayed extinction training in yielding long-term extinction memory, a phenomenon that is referred to as immediate extinction deficit (IED). However, the unknown is whether the IED is just an aberration or continues to affect re-extinction. In Experiment 1, extinction training (1st extinction session) was started at either 1 h (immediate) or 24 h (delayed) after fear conditioning, followed by the 2nd extinction session (re-extinction) 24 h later, and the extinction memory was tested 24 h after the re-extinction. The results showed that rats in the immediate extinction group exhibited no significant reduction of freezing compared with the non-extinguished control after undergoing two extinction training sessions, and exhibited significantly weaker extinction than those animals in the delayed extinction condition, suggesting that the deficit not only occurred in immediate extinction but also in re-extinction. In Experiment 2, rats underwent the same procedures as the immediate extinction groups in Experiment 1, with the exception that they received saline or propranolol (10 mg/kg, i.p.) within minutes after fear conditioning. We found that one injection of propranolol immediately after fear acquisition rescued the deficit of re-extinction but not immediate extinction. This study revealed that the early extinction intervention after severe trauma may not only fail to inhibit the fear response but also act as a secondary trauma which can continually damage the ability to extinguish fear memory. Propranolol may be a good candidate to repair such damage. Our findings improve our understanding of the pathogenesis of PTSD and outcomes of early intervention and may be helpful for selecting appropriate and effective interventions after trauma exposure and avoid secondary trauma that is caused by the intervention itself.

Key words: fear conditioning, extinction, immediate extinction deficit, β-adrenergic receptor antagonist, propranolol