Chronic glucocorticoid deficiency-induced abnormal aggression, autonomic hypoarousal, and social deficit in rats

Research output: Contribution to journalArticle

78 Citations (Scopus)

Abstract

Certain aggression-related psychopathologies are associated with decreased glucocorticoid production and autonomic functions in humans. We have previously shown that experimentally-induced chronic glucocorticoid deficiency leads to abnormal forms of attack in rats. Here, we compared the effects of acute and chronic glucocorticoid deficiency on aggressive behaviour, autonomic responses to challenges, and anxiety. Glucocorticoid synthesis was blocked acutely by the glucocorticoid synthesis blocker metyrapone or chronically by adrenalectomy and low glucocorticoid replacement (ADXr). As shown previously, chronic glucocorticoid deficiency facilitated aberrant attacks directed towards the most vulnerable parts of the opponent's body. The acute inhibition of glucocorticoid synthesis lowered aggressive behaviour without affecting attack targeting. In a different experiment, ADXr rats and their sham-operated controls were exposed to different challenges whereas their heart rate and locomotion were telemetrically recorded. Autonomic responses to social challenges were lowered by chronic, but not by acute glucocorticoid deficiency. Autonomic responses to the elevated plus-maze were only slightly affected by chronic glucocorticoid deficiency. Locomotor behaviour was not affected in either challenge; thus, the altered autonomic reactions were not due to interference from workload. The behaviour of ADXr rats was similar to that of sham-operated controls in the elevated plus-maze, but ADXr rats showed reduced social interactions in the social interaction test. Our data demonstrate that, in rats, chronic but not acute glucocorticoid deficiency induces abnormal attack patterns, deviant cardiovascular responses and social deficits that are similar to those seen in abnormally violent humans. Thus, the similar correlations found in humans probably cover a causal relationship. Experimentally-induced glucocorticoid deficiency may be used to assess the mechanisms underlying glucocorticoid deficiency-induced abnormal forms of aggressiveness.

Original languageEnglish
Pages (from-to)550-557
Number of pages8
JournalJournal of Neuroendocrinology
Volume16
Issue number6
DOIs
Publication statusPublished - Jun 2004

Fingerprint

Aggression
Glucocorticoids
Interpersonal Relations
Metyrapone
Adrenalectomy
Locomotion
Workload
Psychopathology
Human Body
Anxiety
Heart Rate

Keywords

  • Aggression
  • Anxiety
  • Autonomic hypoarousal
  • Glucocorticoids
  • Heart rate

ASJC Scopus subject areas

  • Endocrinology
  • Neuroscience(all)

Cite this

@article{84c2b635d8b345d6ba93fdc2217eef02,
title = "Chronic glucocorticoid deficiency-induced abnormal aggression, autonomic hypoarousal, and social deficit in rats",
abstract = "Certain aggression-related psychopathologies are associated with decreased glucocorticoid production and autonomic functions in humans. We have previously shown that experimentally-induced chronic glucocorticoid deficiency leads to abnormal forms of attack in rats. Here, we compared the effects of acute and chronic glucocorticoid deficiency on aggressive behaviour, autonomic responses to challenges, and anxiety. Glucocorticoid synthesis was blocked acutely by the glucocorticoid synthesis blocker metyrapone or chronically by adrenalectomy and low glucocorticoid replacement (ADXr). As shown previously, chronic glucocorticoid deficiency facilitated aberrant attacks directed towards the most vulnerable parts of the opponent's body. The acute inhibition of glucocorticoid synthesis lowered aggressive behaviour without affecting attack targeting. In a different experiment, ADXr rats and their sham-operated controls were exposed to different challenges whereas their heart rate and locomotion were telemetrically recorded. Autonomic responses to social challenges were lowered by chronic, but not by acute glucocorticoid deficiency. Autonomic responses to the elevated plus-maze were only slightly affected by chronic glucocorticoid deficiency. Locomotor behaviour was not affected in either challenge; thus, the altered autonomic reactions were not due to interference from workload. The behaviour of ADXr rats was similar to that of sham-operated controls in the elevated plus-maze, but ADXr rats showed reduced social interactions in the social interaction test. Our data demonstrate that, in rats, chronic but not acute glucocorticoid deficiency induces abnormal attack patterns, deviant cardiovascular responses and social deficits that are similar to those seen in abnormally violent humans. Thus, the similar correlations found in humans probably cover a causal relationship. Experimentally-induced glucocorticoid deficiency may be used to assess the mechanisms underlying glucocorticoid deficiency-induced abnormal forms of aggressiveness.",
keywords = "Aggression, Anxiety, Autonomic hypoarousal, Glucocorticoids, Heart rate",
author = "J. Haller and J. Hal{\'a}sz and E. Mikics and Kruk, {M. R.}",
year = "2004",
month = "6",
doi = "10.1111/j.1365-2826.2004.01201.x",
language = "English",
volume = "16",
pages = "550--557",
journal = "Journal of Neuroendocrinology",
issn = "0953-8194",
publisher = "Wiley-Blackwell",
number = "6",

}

TY - JOUR

T1 - Chronic glucocorticoid deficiency-induced abnormal aggression, autonomic hypoarousal, and social deficit in rats

AU - Haller, J.

AU - Halász, J.

AU - Mikics, E.

AU - Kruk, M. R.

PY - 2004/6

Y1 - 2004/6

N2 - Certain aggression-related psychopathologies are associated with decreased glucocorticoid production and autonomic functions in humans. We have previously shown that experimentally-induced chronic glucocorticoid deficiency leads to abnormal forms of attack in rats. Here, we compared the effects of acute and chronic glucocorticoid deficiency on aggressive behaviour, autonomic responses to challenges, and anxiety. Glucocorticoid synthesis was blocked acutely by the glucocorticoid synthesis blocker metyrapone or chronically by adrenalectomy and low glucocorticoid replacement (ADXr). As shown previously, chronic glucocorticoid deficiency facilitated aberrant attacks directed towards the most vulnerable parts of the opponent's body. The acute inhibition of glucocorticoid synthesis lowered aggressive behaviour without affecting attack targeting. In a different experiment, ADXr rats and their sham-operated controls were exposed to different challenges whereas their heart rate and locomotion were telemetrically recorded. Autonomic responses to social challenges were lowered by chronic, but not by acute glucocorticoid deficiency. Autonomic responses to the elevated plus-maze were only slightly affected by chronic glucocorticoid deficiency. Locomotor behaviour was not affected in either challenge; thus, the altered autonomic reactions were not due to interference from workload. The behaviour of ADXr rats was similar to that of sham-operated controls in the elevated plus-maze, but ADXr rats showed reduced social interactions in the social interaction test. Our data demonstrate that, in rats, chronic but not acute glucocorticoid deficiency induces abnormal attack patterns, deviant cardiovascular responses and social deficits that are similar to those seen in abnormally violent humans. Thus, the similar correlations found in humans probably cover a causal relationship. Experimentally-induced glucocorticoid deficiency may be used to assess the mechanisms underlying glucocorticoid deficiency-induced abnormal forms of aggressiveness.

AB - Certain aggression-related psychopathologies are associated with decreased glucocorticoid production and autonomic functions in humans. We have previously shown that experimentally-induced chronic glucocorticoid deficiency leads to abnormal forms of attack in rats. Here, we compared the effects of acute and chronic glucocorticoid deficiency on aggressive behaviour, autonomic responses to challenges, and anxiety. Glucocorticoid synthesis was blocked acutely by the glucocorticoid synthesis blocker metyrapone or chronically by adrenalectomy and low glucocorticoid replacement (ADXr). As shown previously, chronic glucocorticoid deficiency facilitated aberrant attacks directed towards the most vulnerable parts of the opponent's body. The acute inhibition of glucocorticoid synthesis lowered aggressive behaviour without affecting attack targeting. In a different experiment, ADXr rats and their sham-operated controls were exposed to different challenges whereas their heart rate and locomotion were telemetrically recorded. Autonomic responses to social challenges were lowered by chronic, but not by acute glucocorticoid deficiency. Autonomic responses to the elevated plus-maze were only slightly affected by chronic glucocorticoid deficiency. Locomotor behaviour was not affected in either challenge; thus, the altered autonomic reactions were not due to interference from workload. The behaviour of ADXr rats was similar to that of sham-operated controls in the elevated plus-maze, but ADXr rats showed reduced social interactions in the social interaction test. Our data demonstrate that, in rats, chronic but not acute glucocorticoid deficiency induces abnormal attack patterns, deviant cardiovascular responses and social deficits that are similar to those seen in abnormally violent humans. Thus, the similar correlations found in humans probably cover a causal relationship. Experimentally-induced glucocorticoid deficiency may be used to assess the mechanisms underlying glucocorticoid deficiency-induced abnormal forms of aggressiveness.

KW - Aggression

KW - Anxiety

KW - Autonomic hypoarousal

KW - Glucocorticoids

KW - Heart rate

UR - http://www.scopus.com/inward/record.url?scp=3042735322&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=3042735322&partnerID=8YFLogxK

U2 - 10.1111/j.1365-2826.2004.01201.x

DO - 10.1111/j.1365-2826.2004.01201.x

M3 - Article

C2 - 15189330

AN - SCOPUS:3042735322

VL - 16

SP - 550

EP - 557

JO - Journal of Neuroendocrinology

JF - Journal of Neuroendocrinology

SN - 0953-8194

IS - 6

ER -