Accession Number:

ADA459042

Title:

Amygdala, Anxiety and Alpha(1) Adrenoceptors: Investigations Utilizing a Rodent Model of Traumatic Stress

Descriptive Note:

Doctoral thesis

Corporate Author:

UNIFORMED SERVICES UNIV OF THE HEALTH SCIENCES BETHESDA MD DEPT OF NEUROLOGY

Personal Author(s):

Report Date:

2006-08-23

Pagination or Media Count:

95.0

Abstract:

Exposure to traumatic stress can result in post-traumatic stress disorder PTSD, characterized by indicators including exaggerated acoustic startle response ASR and alterations in processing of emotional memory. Similar effects can be seen in an animal model of traumatic stress. The basolateral amygdala BLA is an area known to be involved in the processing of emotional memory and startle modulation. Synaptic plasticity in the BLA is thought to play a key part in this memory formation, and therefore can be involved in subsequent stress related pathologies. The first part of this project used this model of traumatic stress to investigate the effects of prazosin, an 1 adrenergic receptor AR antagonist, on stress induced elevation of ASR. This investigation sought to determine its effectiveness in reducing the effects of traumatic stress when given prior to stress. Male Sprague-Dawley rats were injected with 0.5 mgkg iv of prazosin 30 minutes before inescapable tail shock on three consecutive days. ASR testing was performed 1, 4, 7 and 10 days post-stress and compared to baseline and control values. Results show a significant reduction of ASR hyperarousal in the pre-stress injection group. The second part of this project sought to investigate 1A adrenoceptor involvement in long-term potentiation LTP in the BLA and to determine the effects of traumatic stress on this type of plasticity. In the BLA of control animals, the 1A AR specific agonist A61603 1 M completely abolished theta-burst stimulation-induced LTP. In animals previously exposed to a repeated restraint and tailshock stress protocol, only a partial reduction of LTP was detected in the presence of A61603. These findings suggest a possible mechanism contributing to the emotional memory in PTSD and support that the 1A ARs can be a specific pharmacological target in PTSD. Taken together, these findings offer both the possibility of preventative treatment for certain physiological symptoms of PTSD

Subject Categories:

  • Medicine and Medical Research
  • Stress Physiology
  • Pharmacology

Distribution Statement:

APPROVED FOR PUBLIC RELEASE