Effects of fluoxetine on the amygdala and the hippocampus after administration of a single prolonged stress to male Wistar rates: In vivo proton magnetic resonance spectroscopy findings

• Published in: Psychiatry research. Neuroimaging 2015-05, Vol.232 (2), p.154-161
• Main Authors: Han, Fang, Xiao, Bing, Wen, Lili, Shi, Yuxiu
• Format: Article
• Language: English
• Subjects: Amygdala; Amygdala - drug effects; Amygdala - metabolism; Animals; Aspartic Acid - analogs & derivatives; Aspartic Acid - metabolism; Choline - metabolism; Creatine - metabolism; Fluoxetine; Fluoxetine - pharmacology; Fluoxetine - therapeutic use; Hippocampus; Hippocampus - drug effects; Hippocampus - metabolism; Male; Posttraumatic stress disorder; Proton magnetic resonance spectroscopy (1H-MRS); Proton Magnetic Resonance Spectroscopy - methods; Psychiatry; Radiology; Rats; Rats, Wistar; Serotonin Uptake Inhibitors - pharmacology; Serotonin Uptake Inhibitors - therapeutic use; Stress; Stress Disorders, Post-Traumatic - drug therapy; Stress Disorders, Post-Traumatic - metabolism; Stress Disorders, Post-Traumatic - pathology; Stress, Psychological - drug therapy; Stress, Psychological - metabolism; Stress, Psychological - pathology; Treatment Outcome
• ISSN: 0925-4927; 1872-7506
• DOI: 10.1016/j.pscychresns.2015.02.011

Abstract Posttraumatic stress disorder (PTSD) is an anxiety- and memory-based disorder. The hippocampus and amygdala are key areas in mood regulation. Fluoxetine was found to improve the anxiety-related symptoms of PTSD patients. However, little work has directly examined the effects of fluoxetine on the hippocampus and the amygdala. In the present study, male Wistar rats received fluoxetine or vehicle after exposure to a single prolonged stress (SPS), an animal model of PTSD. In vivo proton magnetic resonance spectroscopy (1 H-MRS) was performed −1, 1, 4, 7 and 14 days after SPS to examine the effects of fluoxetine on neurometabolite changes in amygdala, hippocampus and thalamus. SPS increased the N -acetylaspartate (NAA)/creatine (Cr) and choline moieties (Cho)/Cr ratios in the bilateral amygdala on day 4, decreased the NAA/Cr ratio in the left hippocampus on day 1, and increased both ratios in the right hippocampus on day 14. But no significant change was found in the thalamus. Fluoxetine treatment corrected the SPS increases in the NAA/Cr and Cho/Cr levels in the amygdala on day 4 and in the hippocampus on day 14, but it failed to normalise SPS-associated decreases in NAA/Cr levels in the left hippocampus on day 1. These results suggested that metabolic abnormalities in the amygdala and the hippocampus were involved in SPS, and different effects of fluoxetine in correcting SPS-induced neurometabolite changes among the three areas. These findings have implications for fluoxetine treatment in PTSD.