Aggression in men may be due to variations in one of two genes involved in the activity of the neurotransmitter serotonin, according to results of a study reported at the 6th International Congress of Neuroendocrinology (ICN 2006), which takes place June 19 – 22 at the David L. Lawrence Convention Center in downtown Pittsburgh.
However, men with the “aggression” genes aren’t necessarily all cads; genetics appears to be predictive only if men have hostile attitudes and fathers who never completed high school. Moreover, a genetic predisposition toward aggression could be rebuffed by a mother who nurtures her infant, suggests another study involving primates.
Summaries of these studies’ findings and research revealing new information about the molecular and biophysical mechanisms that determine sexual arousal and sexual behavior follow:
No argument here: Research determining why some men are more aggressive
What pushes some men to the outer limits of machismo, to be more confrontational or apt to get into scuffles and arguments? According to results of a study involving 531 white men of European descent, belligerence may be attributable to variations in one of two genes involved in the activity of the neurotransmitter serotonin. However, men with the “aggression” genes aren’t necessarily all cads, cautions Stephen Manuck, Ph.D., professor of psychology at the University of Pittsburgh, who led the research. Genetics appears to be predictive of aggression only if men also have more cynical and hostile attitudes toward others or fathers who never completed high school.
The Pitt study is the first to look at whether aggression in “normal” men may, in part, be attributed to the same serotonin-related genetic alterations that have been associated with aggressive behaviors in certain psychiatric and criminal populations. Indeed, the study found those who reported past fights, conflicts with authority figures or breaking objects in bouts of anger were more likely to carry the “low activity” MAOA gene variant that’s been linked to criminal violence.
Monoamine oxidase-A, or MAOA, is an enzyme that inactivates serotonin, helping to keep its levels in proper balance. Yet the low activity MAOA gene was only associated with aggressive “acting out” among men with oppositional attitudes. Variation in another serotonin gene, the serotonin 2A receptor, which is necessary for the neurotransmitter to act, also was predictive of antagonistic behavior, but only among men whose fathers had less than a high-school education. The same gene has been implicated in personality and anti-social disorders and in some criminal offenders.
Maternal buffer can prevent aggression
It can be a real jungle out there, and parents often do their best to shield their children from the worst of influences. According to new research, mothers can offer some added protection that fathers can’t: a buffer against the development of aggressive behavior. According to primate studies, those with a genetic susceptibility for hostile behavior can grow up to be docile in nature, provided they had loving and caring mothers as infants.
Up to 10 percent of rhesus monkeys living in the wild are overly aggressive and react inappropriately even in the most benign situations, a trait they typically develop at a young age and seldom grow out of. Moreover, researchers have recently found, these aggressive animals have lower levels of the brain chemical serotonin, an observation noted through adulthood. Like their wild counterparts, monkeys studied in the laboratory that have a variation of a certain serotonin-related gene also make less serotonin and are more impulsive and aggressive, but only if they had mothers who did not bond with them as infants. As Stephen J. Suomi, Ph.D., chief, Laboratory of Comparative Ethology at the National Institute of Child Health & Human Development, has demonstrated, monkeys with the same gene-based serotonin deficiency who were reared by more nurturing mothers avoid developing aggressive behaviors. “Maternal buffering,” he suggests, can trump genetics. The same may be true in humans.
Getting to the essential mechanisms of brain arousal and sexual behavior
To understand what brings about arousal of the central nervous system leading to sexual behavior, scientists have had to discover specific biochemical reactions within a select group of neurons in the hypothalamus, says Donald Pfaff, Ph.D., professor and head of the Laboratory of Neurobiology and Behavior at Rockefeller University. The process involves a complement of sex steroid hormones, perhaps as many as 120 genes and a host of environmental variables (not least among them, arousing stimuli and a suitable mate).
In these brain mechanisms, interactions between genes and the immediate environment play an essential part. Other, longer-term interactions stem from an animal’s treatment about the time of birth. Those longer-term interactions are hypothesized to depend on chemical modification of either DNA through a process called methylation or of proteins covering the DNA. These so-called epigenetic mechanisms can produce heritable changes in behaviors without changing the animal’s DNA sequence. Dr. Pfaff’s new results reveal some of the molecular and biophysical mechanisms that dictate when and how chemical messages for generalized arousal affect the neurons in the hypothalamus that control sexual arousal and sexual behaviors.
Held in a different part of the world every four years under the auspices of the International Neuroendocrine Federation, this year’s congress – Bridging Neuroscience and Endocrinology – is being sponsored by the American Neuroendocrine Society and the University of Pittsburgh School of Medicine. The first full day of the program, June 20, is being held in conjunction with the 10th Annual Meeting of the Society for Behavioral Neuroendocrinology.
Formerly the International Society of Neuroendocrinology, the International Neuroendocrine Federation consists of six member societies and seven regional groups, representing all parts of the world. The federation’s president is John A. Russell, MBChB, Ph.D., chair of neuroendocrinology, University of Edinburgh. The chair of the ICN 2006 scientific program is Iain J. Clarke, Ph.D., professorial fellow in the department of physiology at Monash University in Australia. Tony Plant, Ph.D., professor of cell biology and physiology and director of the Center for Research in Reproductive Physiology, University of Pittsburgh School of Medicine, is chair of the local organizing committee.
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