Abstract
Over the last two decades, the study of the relationship between nature and nurture in shaping human behavior has encountered a renewed interest. Behavioral genetics showed that distinct polymorphisms of genes that code for proteins that control neurotransmitter metabolic and synaptic function are associated with individual vulnerability to aversive experiences, such as stressful and traumatic life events, and may result in an increased risk of developing psychopathologies associated with violence. On the other hand, recent studies indicate that experiencing aversive events modulates gene expression by introducing stable changes to DNA without modifying its sequence, a mechanism known as “epigenetics”. For example, experiencing adversities during periods of maximal sensitivity to the environment, such as prenatal life, infancy and early adolescence, may introduce lasting epigenetic marks in genes that affect maturational processes in brain, thus favoring the emergence of dysfunctional behaviors, including exaggerate aggression in adulthood. The present review discusses data from recent research, both in humans and animals, concerning the epigenetic regulation of four genes belonging to the neuroendocrine, serotonergic and oxytocinergic pathways—Nuclear receptor subfamily 3-group C-member 1 (NR3C1), oxytocin receptor (OXTR), solute carrier-family 6 member 4 (SLC6A4) and monoamine oxidase A (MAOA)—and their role in modulating vulnerability to proactive and reactive aggressive behavior. Behavioral genetics and epigenetics are shedding a new light on the fine interaction between genes and environment, by providing a novel tool to understand the molecular events that underlie aggression. Overall, the findings from these studies carry important implications not only for neuroscience, but also for social sciences, including ethics, philosophy and law.
Highlights
Over the last two decades, the study of the relationship between nature and nurture in shaping human behavior has encountered a renewed interest
Behavioral genetics showed that distinct polymorphisms of genes that code for proteins that control neurotransmitter metabolic and synaptic function are associated with individual vulnerability to aversive experiences, such as stressful and traumatic life events, and may result in an increased risk of developing psychopathologies associated with violence
Neuroscientific research has focused more and more on the biological mechanisms that predispose to behavioral disorders as a consequence of the exposure to aversive environments
Summary
Studies both in animals (Mosaferi et al, 2015) and humans (McEwen et al, 2012) indicate that the environment, mostly during prenatal stage and infancy, impact significantly on neural development, as several critical periods with lasting consequences on behavior have been documented (Stiles and Jernigan, 2010). In juvenile and adult male rats, for example, an increased number of physical attacks toward inoffensive peers and females have been predicted by repeated maternal separation in the first 2 weeks of life or by post-weaning social isolation (Haller et al, 2014) In rats, both prenatal and early postnatal stressors, like physical restraint during pregnancy or repeated maternal separation after birth, interfere with normal cell proliferation and differentiation and with dendritic formation, leading to altered neural circuits that may result in exaggerate aggressive behaviors (Lukas et al, 2010; de Souza et al, 2013). Talking about aggressive behavior predisposition, a role has been described to date only for DNA methylation and histone acetylation, whose scientific evidence in literature is reviewed below
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