Testosterone, cortisol, and serotonin as key regulators of social aggression: A review and theoretical perspective

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Abstract

In human and non-human animals the steroid hormones cortisol and testosterone are involved in social aggression and recent studies suggest that these steroids might jointly regulate this behavior. It has been hypothesized that the imbalance between cortisol and testosterone levels is predictive for aggressive psychopathology, with high testosterone to cortisol ratio predisposing to a socially aggressive behavioral style. In this review, we focus on the effects of cortisol and testosterone on human social aggression, as well as on how they might modulate the aggression circuitry of the human brain. Recently, serotonin is hypothesized to differentiate between impulsive and instrumental aggression, and we will briefly review evidence on this hypothesis. The aim of this article is to provide a theoretical framework for the role of steroids and serotonin in impulsive social aggression in humans.

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Two receptor systems for corticosterone in rat brain: microdistribution and differential occupation.

J Reul, E. de Kloet (1985)

Two receptor systems for corticosterone (CORT) can be distinguished in rat brain: mineralocorticoid-like or CORT receptors (CR) and glucocorticoid receptors (GR). The microdistribution and extent of occupation of each receptor population by CORT were studied. The CR system is restricted predominantly to the lateral septum and hippocampus. Within the hippocampus, the highest density occurs in the subiculum +/- CA1 cell field (144 fmol/mg protein) and the dentate gyrus (104 fmol/mg protein). Affinity of CR for CORT was very high (Kd, approximately 0.5 nM). The GR system has a more widespread distribution in the brain. The highest density for GR is in the lateral septum (195 fmol/mg protein), the dentate gyrus (133 fmol/mg protein), the nucleus tractus solitarii and central amygdala. Substantial amounts of GR are present in the paraventricular nucleus and locus coeruleus and low amounts in the raphe area and the subiculum + CA1 cell field. The affinity of GR for CORT (Kd, approximately 2.5-5 nM) was 6- to 10-fold lower than that of CR. Occupation of CR by endogenous ligand was 89.5% during morning trough levels of pituitary-adrenal activity (plasma CORT, 1.4 micrograms/100 ml). Similar levels of occupation (88.7% and 97.6%) were observed at the diurnal peak (plasma CORT, 27 micrograms/100 ml) and after 1 h of restraint stress (plasma CORT, 25 micrograms/100 ml), respectively. Furthermore, a dose of 1 microgram CORT/100 g BW, sc, resulted in 80% CORT receptor occupation, whereas GR were not occupied. For 50% occupation of GR, doses needed to be increased to 50-100 micrograms/100 g BW, and for 95% occupation, a dose of 1 mg CORT was required. The plasma CORT level at the time of half-maximal GR occupation was about 25 micrograms/100 ml, which is in the range of levels attained after stress or during the diurnal peak of pituitary-adrenal activity. Thus, CR are extensively filled (greater than 90%) with endogenous CORT under most circumstances, while GR become occupied concurrent with increasing plasma CORT concentrations due to stress or diurnal rhythm. We conclude that CORT action via CR may be involved in a tonic (permissive) influence on brain function with the septohippocampal complex as a primary target. In view of the almost complete occupation of CR by endogenous hormones, the regulation of the CORT signal via CR will, most likely, be by alterations in the number of such receptors. In contrast, CORT action via GR is involved in its feedback action on stress-activated brain mechanisms, and GR occur widely in the brain.(ABSTRACT TRUNCATED AT 400 WORDS)

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Insensitivity to future consequences following damage to human prefrontal cortex.

A Bechara, A Damasio, H. Damasio … (2015)

Following damage to the ventromedial prefrontal cortex, humans develop a defect in real-life decision-making, which contrasts with otherwise normal intellectual functions. Currently, there is no neuropsychological probe to detect in the laboratory, and the cognitive and neural mechanisms responsible for this defect have resisted explanation. Here, using a novel task which simulates real-life decision-making in the way it factors uncertainty of premises and outcomes, as well as reward and punishment, we find that prefrontal patients, unlike controls, are oblivious to the future consequences of their actions, and seem to be guided by immediate prospects only. This finding offers, for the first time, the possibility of detecting these patients' elusive impairment in the laboratory, measuring it, and investigating its possible causes.

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Neural mechanisms of aggression.

Randy J Nelson, Brian Trainor (2007)

Unchecked aggression and violence exact a significant toll on human societies. Aggression is an umbrella term for behaviours that are intended to inflict harm. These behaviours evolved as adaptations to deal with competition, but when expressed out of context, they can have destructive consequences. Uncontrolled aggression has several components, such as impaired recognition of social cues and enhanced impulsivity. Molecular approaches to the study of aggression have revealed biological signals that mediate the components of aggressive behaviour. These signals may provide targets for therapeutic intervention for individuals with extreme aggressive outbursts. This Review summarizes the complex interactions between genes, biological signals, neural circuits and the environment that influence the development and expression of aggressive behaviour.

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Author and article information

Contributors

: E.R.Montoya@uu.nl

Journal

Journal ID (nlm-ta): Motiv Emot

Title: Motivation and Emotion

Publisher: Springer US (Boston )

ISSN (Print): 0146-7239

ISSN (Electronic): 1573-6644

Publication date (Electronic): 25 November 2011

Publication date PMC-release: 25 November 2011

Publication date (Print): March 2012

Volume: 36

Issue: 1

Pages: 65-73

Affiliations

[1 ]Department of Experimental Psychology, Utrecht University, Utrecht, The Netherlands

[2 ]Department of Psychiatry and Mental Health, University of Cape Town, Cape Town, South Africa

Article

Publisher ID: 9264

DOI: 10.1007/s11031-011-9264-3

PMC ID: 3294220

PubMed ID: 22448079

SO-VID: 96ca525d-3cee-45bc-babf-3ed97531dea7

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ScienceOpen disciplines: Clinical Psychology & Psychiatry

Keywords: serotonin,cortisol,testosterone,instrumental aggression,impulsive aggression

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ScienceOpen disciplines: Clinical Psychology & Psychiatry

Keywords: serotonin, cortisol, testosterone, instrumental aggression, impulsive aggression

Testosterone, cortisol, and serotonin as key regulators of social aggression: A review and theoretical perspective

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Serotonin and BEYOND

Most cited references 77

Two receptor systems for corticosterone in rat brain: microdistribution and differential occupation.

Insensitivity to future consequences following damage to human prefrontal cortex.

Neural mechanisms of aggression.

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