Klaus A. Miczek, Margaret Haney, Jennifer Tidey, Jeffrey Vivian, and Elise Weerts
Violence and aggression like all other behaviors are ultimately a function of brain activity. The evolution of brain mechanisms that mediate aggressive and violent behaviors may be traced from humans to other animal species, and most of the neurochemical and neuropharmacologic evidence stems from studies with non-human species. The relevant neurochemical systems start with genetic instructions, undergo critical maturation periods, and—as evidence during the past two decades demonstrates—environmental, social, nutritional, and experiential factors modulate these systems continuously.
Insight into the neurochemical mechanisms of violence in humans has been obtained only indirectly by correlating biochemical markers in peripheral fluids or in the spinal cord with past behavioral events. In the meantime, an explosion of neuroscience research continuously informs on highly discrete neuroanatomical processes, pools of synthetic and metabolic enzymes, exquisitely regulated neural receptor populations, and transducer systems. None of these newly developed research methods have been applied to the issues of violence as of yet.
Klaus Miczek, Margaret Haney, Jennifer Tidey, Jeffrey Vivian, and Elise Weerts are at the Department of Psychology, Tufts University.
Up to the 1960s, the canonical transmitter substances such as norepinephrine (NE), dopamine (DA), serotonin (5-hydroxytryptamine, 5-HT), and acetylcholine (ACh) were the major focus of neuroscience research. Accelerating since the 1970s has been the research on receptor subtypes for endogenous neurotransmitters and neuromodulators and for psychoactive drugs. The discovery of peptides and steroids in the brain, as well as their neural receptors, prompts the consideration of possible new mechanisms that may be relevant to aggressive and violent behavior. In the early zeal, neuroscience research attempted to discover the ''chemical code" of specific behavioral functions; noradrenergic feeding and cholinergic drinking were initial examples of normal homeostatic functions, the dopamine hypothesis of schizophrenia was advanced, and serotonin was sometimes referred to as a "civilizing neurohumor" keeping sex and aggression under control. However, by now, nearly every neurotransmitter has been implicated in the neural mechanisms for these complex physiologic and behavioral phenomena, and this applies also to aggressive and violent behavior. It is highly unlikely that the problem of violence can be reduced to a dysfunction in a single enzyme, receptor, or molecular component of a nerve cell. The present framework for studies on neurochemical mechanisms of violence distinguishes a neurochemical profile of individuals with an aggressive "trait" from those events that mediate the initiation, execution, and termination of aggressive and violent acts on a moment-to-moment "state" basis. The latter are significant in the development of rational therapeutic interventions. In general, clinical studies focus on biochemical markers of aggression, or violence as a trait, whereas experimental studies in animals provide mostly data on the proximal antecedents and consequences of aggressive behavior (state). Genetic studies of aggressive traits in animals have only rarely included concurrent assessments of their biochemical basis (see Carey, in this volume).
It has become a truism to point out that each type of violent and aggressive behavior is associated with distinctive neurochemical changes, and more selective logical interventions modulate these different behavior patterns in an increasingly specific manner. In order to appreciate the range of aggressive and violent behaviors at the animal and human level that have been studied for their neurochemical basis, it will be useful to briefly summarize the major animal models as well as clinical types of aggression and violence.