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Review
. 2019 Dec 4:10:872.
doi: 10.3389/fpsyt.2019.00872. eCollection 2019.

Neurobiology of Aggressive Behavior-Role of Autoantibodies Reactive With Stress-Related Peptide Hormones

Affiliations
Review

Neurobiology of Aggressive Behavior-Role of Autoantibodies Reactive With Stress-Related Peptide Hormones

Henning Vaeroy et al. Front Psychiatry. .

Abstract

Adrenocorticotropic hormone together with arginine vasopressin and oxytocin, the neuropeptides regulating the stress response and the hypothalamic-pituitary-adrenal axis activity, are known to modulate aggressive behavior. The functional role of the adrenocorticotropic hormone immunoglobulin G autoantibodies in peptidergic signaling and motivated behavior, including aggression, has been shown in experimental and in vitro models. This review summarizes some experimental data implicating autoantibodies reactive with stress-related peptides in aggressive behavior.

Keywords: adrenocorticotropic hormone; autoantibodies; cortisol; epitopes; human aggression; hypothalamic-pituitary-adrenal axis; oxytocin; vasopressin.

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Figures

Figure 1
Figure 1
Plasma ACTH-reactive IgG modulate ACTH-induced cortisol secretion. Legend to Figure 1 . ACTH-reactive IgG are naturally present in human plasma and modulate ACTH-induced cortisol secretion depending on the ACTH binding epitope. In the non-aggressive subjects IgG bind mainly the central part (11–24) of ACTH, containing the MC2R pharmacophore, while IgG in violent aggressors display increased affinity for ACTH and bind mainly its N-terminal part (1–13). Some IgG from both the non-aggressive and aggressive study persons have both been shown to prevent ACTH-induced cortisol secretion from the adrenal cortex cells, such inhibitory effect was associated with low IgG binding to the central ACTH part (11–24), i.e. similar to the binding pattern characterizing IgG of violent aggressors (34).

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References

    1. Groves CL, Anderson CA. Aversive events and aggression. Curr Opin In Psychol (2018) 19:144–8. 10.1016/j.copsyc.2017.03.027 - DOI - PubMed
    1. Bettencourt B, Miller N. Gender differences in aggression as a function of provocation: a meta-analysis. Psychol Bull (1996) 119(3):422. 10.1037/0033-2909.119.3.422 - DOI - PubMed
    1. Bosma H, Marmot MG, Hemingway H, Nicholson AC, Brunner E, Stansfeld SA. Low job control and risk of coronary heart disease in Whitehall II (prospective cohort) study. BMJ (1997) 314(7080):558. 10.1136/bmj.314.7080.558 - DOI - PMC - PubMed
    1. Templin C, Ghadri JR, Diekmann J, Napp LC, Bataiosu DR, Jaguszewski M, et al. Clinical features and outcomes of Takotsubo (stress) cardiomyopathy. N Engl J Med (2015) 373(10):929–38. 10.1056/NEJMoa1406761 - DOI - PubMed
    1. Keynejad RC, Frodl T, Kanaan R, Pariante C, Reuber M, Nicholson TR. Stress and functional neurological disorders: mechanistic insights. J Neurol Neurosurg Psychiatry (2019) 90(7):813–21. 10.1136/jnnp-2018-318297 - DOI - PubMed

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