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

E. Mikics, M. Tóth, Patrícia Varjú, B. Gereben, Z. Liposits, Mária Ashaber, J. Halász, I. Barna, Imre Farkas, J. Haller

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)1198-1210
Number of pages13
JournalPsychoneuroendocrinology
Volume33
Issue number9
DOIs
Publication statusPublished - Oct 2008

Fingerprint

Social Behavior
Amygdala
Foot
Shock
Interpersonal Relations
Wounds and Injuries
Messenger RNA
Neuronal Plasticity
Locus Coeruleus
Brain
Prefrontal Cortex
Fear
Real-Time Polymerase Chain Reaction
Immunohistochemistry
Central Amygdaloid Nucleus
Basolateral Nuclear Complex

Keywords

  • Amygdala
  • CRF
  • NK1 receptor
  • PTSD
  • Social behavior
  • Trauma

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism
  • Psychiatry and Mental health
  • Biological Psychiatry
  • Endocrine and Autonomic Systems
  • Psychology(all)

Cite this

@article{159c579c2bf6426fa5ca4461615d7a8c,
title = "Lasting changes in social behavior and amygdala function following traumatic experience induced by a single series of foot-shocks",
abstract = "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.",
keywords = "Amygdala, CRF, NK1 receptor, PTSD, Social behavior, Trauma",
author = "E. Mikics and M. T{\'o}th and Patr{\'i}cia Varj{\'u} and B. Gereben and Z. Liposits and M{\'a}ria Ashaber and J. Hal{\'a}sz and I. Barna and Imre Farkas and J. Haller",
year = "2008",
month = "10",
doi = "10.1016/j.psyneuen.2008.06.006",
language = "English",
volume = "33",
pages = "1198--1210",
journal = "Psychoneuroendocrinology",
issn = "0306-4530",
publisher = "Elsevier Limited",
number = "9",

}

TY - JOUR

T1 - Lasting changes in social behavior and amygdala function following traumatic experience induced by a single series of foot-shocks

AU - Mikics, E.

AU - Tóth, M.

AU - Varjú, Patrícia

AU - Gereben, B.

AU - Liposits, Z.

AU - Ashaber, Mária

AU - Halász, J.

AU - Barna, I.

AU - Farkas, Imre

AU - Haller, J.

PY - 2008/10

Y1 - 2008/10

N2 - 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.

AB - 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.

KW - Amygdala

KW - CRF

KW - NK1 receptor

KW - PTSD

KW - Social behavior

KW - Trauma

UR - http://www.scopus.com/inward/record.url?scp=51249102385&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=51249102385&partnerID=8YFLogxK

U2 - 10.1016/j.psyneuen.2008.06.006

DO - 10.1016/j.psyneuen.2008.06.006

M3 - Article

C2 - 18656313

AN - SCOPUS:51249102385

VL - 33

SP - 1198

EP - 1210

JO - Psychoneuroendocrinology

JF - Psychoneuroendocrinology

SN - 0306-4530

IS - 9

ER -