Lasting changes in social behavior and amygdala function following traumatic experience induced by a single series of foot-shocks

• Published in: Psychoneuroendocrinology Vol. 33; no. 9; pp. 1198 - 1210
• Main Authors: Mikics, Éva, Tóth, Máté, Varjú, Patrícia, Gereben, Balázs, Liposits, Zsolt, Ashaber, Mária, Halász, József, Barna, István, Farkas, Imre, Haller, József
• Format: Journal Article
• Language: English
• Published: Oxford Elsevier Ltd 01.10.2008; Elsevier
• Subjects: Adult and adolescent clinical studies; Amygdala; Amygdala - physiology; Analysis of Variance; Animals; Anxiety disorders. Neuroses; Avoidance Learning - physiology; Behavioral psychophysiology; Biological and medical sciences; Corticotropin-Releasing Hormone - genetics; Corticotropin-Releasing Hormone - metabolism; CRF; Endocrinology & Metabolism; Fundamental and applied biological sciences. Psychology; Gene Expression Regulation - physiology; Hormones and behavior; Male; Medical sciences; NK1 receptor; Norepinephrine - metabolism; Post-traumatic stress disorder; Prefrontal Cortex - metabolism; Proto-Oncogene Proteins c-fos - genetics; Proto-Oncogene Proteins c-fos - metabolism; Psychiatry; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; Psychopathology. Psychiatry; PTSD; Rats; Rats, Wistar; Receptors, Neurokinin-1 - genetics; Receptors, Neurokinin-1 - metabolism; RNA, Messenger - analysis; Serotonin - metabolism; Social Behavior; Statistics, Nonparametric; Stress, Psychological - physiopathology; Trauma; PTSD; Social behavior; Amygdala; NK1 receptor; Trauma; CRF; Shock; NK1 Tachykinin receptor; Central nervous system; Anxiety disorder; Corticotropin releasing factor; Behavior change; Basal ganglion; Posttraumatic stress disorder; Stress; Encephalon; Foot; Hypothalamic hormone; Social interaction; Hormone releasing factor; Amygdaloid nucleus
• ISSN: 0306-4530; 1873-3360
• DOI: 10.1016/j.psyneuen.2008.06.006

Summary Neuronal plasticity within the amygdala mediates many behavioral effects of traumatic experience, and this brain region also controls various aspects of social behavior. However, the specific involvement of the amygdala in trauma-induced social deficits has never been systematically investigated. We exposed rats to a single series of electric foot-shocks – a frequently used model of trauma – and studied their behavior in the social avoidance and psychosocial stimulation tests (non-contact versions of the social interaction test) at different time intervals. Social interaction-induced neuronal activation patterns were studied in the prefrontal cortex (orbitofrontal and medial), amygdala (central, medial, and basolateral), dorsal raphe and locus coeruleus. Shock exposure markedly inhibited social behavior in both tests. The effect lasted at least 4 weeks, and amplified over time. As shown by c-Fos immunocytochemistry, social interactions activated all the investigated brain areas. Traumatic experience exacerbated this activation in the central and basolateral amygdala, but not in other regions. The tight correlation between the social deficit and amygdala activation patterns suggest that the two phenomena were associated. A real-time PCR study showed that CRF mRNA expression in the amygdala was temporarily reduced 14, but not 1 and 28 days after shock exposure. In contrast, amygdalar NK1 receptor mRNA expression increased throughout. Thus, the trauma-induced social deficits appear to be associated with, and possibly caused by, plastic changes in fear-related amygdala subdivisions.