Genetic and Epigenetic Determinants of Aggression

  • Barbara Klausz
  • József Haller
  • Áron Tulogdi
  • Dóra Zelena


Every year many people worldwide die because of assault, and many more become victims of aggressive behavior including terrorism and hooliganism. Although aggression is an adaptive response to social challenges of the environment, pathological forms, mostly associated with other psychological disturbances, are highly destructive. Several brain regions (like hypothalamic attach are, medial amygdala, periaqueductal gray) and several molecules (testosterone, serotonin, vasopressin, etc.) are involved in the development of this behavior, but one of the most important determinants is the behavior of the encounter. Therefore, it is not surprising that epigenetic changes, connecting environment with gene activation, could be highly involved in fine-tuning the brain structures and molecular network taking part in aggression. In the last few decades, a lot of knowledge accumulated about epigenetic modification during development and in cancer formation; however, little is known about the role of epigenetic changes in mature cells. In this chapter, we summarize the available evidence on connection between aggression and genetic and epigenetic modification. One of the main determinants of this behavior, testosterone acts—at least partly—on epigenome. Other important contributors, like parts of the serotonergic system, vasopressin, and neurotrophins, underwent epigenetic regulations. Moreover, inhibition of histone deacetylase influences the aggressive behavior of animals. All the reviewed studies support the importance of genetic and epigenetic changes in the development of aggression.



Serotonin receptor


Serotonin transporter






Atrial natriuretic peptide


Androgen receptor


Arginine vasopressin


Brain-derived neurotrophic factor


Bed nucleus of stria terminalis


Calcium/calmodulin-dependent kinase


Central amygdala


Central nervous system




Cytosine–guanine dinucleotide


Corticotropin-releasing hormone


Dopamine D2-receptor


Dopamine beta-hydroxylase


DNA methyltransferase


Estrogen receptor


Estrogen receptor-α


Gamma-aminobutyric acid


Glucocorticoid receptor


Hypothalamic attack area


Histone acetyltransferase


Histone deacetylase

HPA axis

Hypothalamo–pituitary–adrenocortical axis






Long variant of the 5-HTT


Monoamine oxidase


Medial amygdala




Medial preoptic area


Methylenetetrahydrofolate reductase




Neural cell adhesion molecule


Nerve growth factor


Neurokinin1, the receptor for substance P


Nitric oxide


Nitric oxide synthase




Periaqueductal gray


Prefrontal cortex




Nucleus paraventricularis hypothalami


Short variant of the 5-HTT






Supraoptic nucleus


Transforming growth factor-α


Tryptophan hydroxylase


Vasopressin V1a receptor valValine


Ventromedial nucleus of the hypothalamus




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Copyright information

© Springer Science+Business Media, LLC 2012

Authors and Affiliations

  • Barbara Klausz
    • 1
  • József Haller
    • 1
  • Áron Tulogdi
    • 1
  • Dóra Zelena
    • 1
  1. 1.Department of Behavioural Neurobiology, Laboratory of Behavioural and Stress Studies, Institute of Experimental MedicineHungarian Academy of SciencesBudapestHungary

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