Opiate Masking of Stress-induced Hypervigilance: The Cause of Delayed Symptom Presentation in PTSD
Abstract
Post-traumatic stress disorder is a multi-symptom psychological disorder that includes, as one possible symptom, an exaggerated startle response [1-4]. As has been reported in longitudinal human studies, the change in startle reactivity occurs over a period of time following the associated trauma [5]. Increases in startle magnitudes can be elicited in rats by exposing them to inescapable shock, but, like the disorder, the change in this reflex response does not occur for a few days [6-9]. In contrast, startle response magnitude can be elicited within several minutes pharmacologically using several compounds, most notably corticotrophin-releasing hormone (CRH)[10-13]. CRH is a key element for the stress response as it is involved in communicating between centers of the brain that organize the autonomic and endocrine responses [14;15], and it is elevated in rats in the for several hours following shock exposure [16]. Given the discrepancy in the timing of stress-enhanced startle reactivity and CRH-enhanced startle reactivity, we hypothesized that there may be an additional physiological response to the stressor that overrides and masks the exaggerated startle that should be evident shortly after CRH is elevated. Likely candidates such a masking role are the endogenous opiates. In contrast, if it is shown that a delayed-expression exaggerated startle response can be elicited after exposure to a predictable and controllable stressor, then we would have to consider an alternative to the masking agent hypothesis.
Document Details
- Document Type
- Technical Report
- Publication Date
- Apr 01, 2010
- Accession Number
- ADA538726
Entities
People
- Kevin D. Beck
Organizations
- Veterans Administration Medical Center