Genetic and Epigenetic Determinants of Aggression

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

Abstract

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.

Abbreviations

5-HT-R

Serotonin receptor

5-HTT

Serotonin transporter

ACTH

Adrenocorticotropin

ADX

Adrenalectomy

ANP

Atrial natriuretic peptide

AR

Androgen receptor

AVP

Arginine vasopressin

BDNF

Brain-derived neurotrophic factor

BNST

Bed nucleus of stria terminalis

CaMK

Calcium/calmodulin-dependent kinase

CeA

Central amygdala

CNS

Central nervous system

COMT

Catechol-O-methyltransferase

CpG

Cytosine–guanine dinucleotide

CRH

Corticotropin-releasing hormone

D2-R

Dopamine D2-receptor

DBH

Dopamine beta-hydroxylase

DNMT

DNA methyltransferase

ER

Estrogen receptor

ERα

Estrogen receptor-α

GABA

Gamma-aminobutyric acid

GR

Glucocorticoid receptor

HAA

Hypothalamic attack area

HAT

Histone acetyltransferase

HDAC

Histone deacetylase

HPA axis

Hypothalamo–pituitary–adrenocortical axis

IL-6

Interleukin-6

KO

Knockout

L

Long variant of the 5-HTT

MAO

Monoamine oxidase

MeA

Medial amygdala

met

Methionine

MPOA

Medial preoptic area

MTHFR

Methylenetetrahydrofolate reductase

NA

Noradrenaline

NCAM

Neural cell adhesion molecule

NGF

Nerve growth factor

NK1

Neurokinin1, the receptor for substance P

NO

Nitric oxide

NOS

Nitric oxide synthase

OT

Oxytocin

PAG

Periaqueductal gray

PFC

Prefrontal cortex

POMC

Proopiomelanocortin

PVN

Nucleus paraventricularis hypothalami

S

Short variant of the 5-HTT

sc

Subcutaneous

SER

Serotonin

SON

Supraoptic nucleus

TGFα

Transforming growth factor-α

TH

Tryptophan hydroxylase

V1a-R

Vasopressin V1a receptor valValine

VMH

Ventromedial nucleus of the hypothalamus

VPA

Valproate

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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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