ABSTRACT
Aggression can be defined as 'behavior intended to harm another' which can be seen both from humans and animals. However, trying to understand aggression in a simplistic view may make it difficult to develop an integrated approach. So, we tried to explain aggression in a multidisciplinary approach, affected by various factors such as neuroanatomical structures, neurotransmitter, genes, and sex hormone. Parallel with animal models, human aggression can be understood with two phenomena, offensive aggression and defensive aggression. Neurobiological model of aggression give a chance to explain aggression with an imbalance between prefrontal regulatory influences and hyper-reactivity of the subcortical areas involved in affective evaluation, finally in an aspect of brain organization. Serotonin and GABA usually inhibit aggression and norepinephrine while glutamate and dopamine precipitate aggressive behavior. As there is no one gene which has been identified as a cause of aggression, functions between gene to gene interaction and gene to environment interaction are being magnified. Contributions of sex hormone to aggression, especially molecular biologic interaction of testosterone and regulation of estrogen receptor have been emphasized during the research on aggression. This multidisciplinary approach on aggression with types, neurochemical bases, and animal models can bring integrated interpretation on aggression.
Subject(s)
Animals , Humans , Aggression , Brain , Dopamine , Estrogens , gamma-Aminobutyric Acid , Glutamic Acid , Models, Animal , Neurobiology , Neurotransmitter Agents , Norepinephrine , Serotonin , TestosteroneABSTRACT
An association study with Korean schizophrenic patients(N=84) and normal controls(N=87) was performed to find the relationship between catechol-o-methyltransferase(COMT) gene polymorphism and schizophrenia using polymerase chain reaction-restriction fragment length polymorphism. When we compared the allele and genotype frequencies of Bg/I COMT gene polymorphism in schizophrenics and normal controls, there was no significant difference between two groups. Our results do not support an association between the Bg/I polymorphism of COMT gene and schizophrenia.