KristyK3211

Hello, I am using this page to experiment with data that I am interested in putting on Wikipedia.

Kristy, if you look at the "edit this page" my changes make sense; but they obviously don't when looking at the final version. I suspect i did something wrong when trying to put in references. So, i'm going to give the refs here and let you put them in:

for the critique of the use of animal behavior as applied to humans: Zuk, M. "Sexual Selections: What We Can and Can't Learn about Sex from Animals." University of California Press, 2002

for the critique of evolutionary explanations of human behavior, especially with regard to sex diffs: Hubbard, R. "Have Only Men Evolved?" in The Gender of Science, Ed. J. A. Kourany, Prentice Hall, 2002

Hrdy, S. B. "Empathy, Polyandry, and the Myth of the Coy Female" in The Gender of Science, Ed. J. A. Kourany, Prentice Hall, 2002

That seems to have fixed it! Sorry for the screw up.

Evolution of Aggression

Aggression within a Species

Aggression against conspecifics serves a number of purposes having to do with breeding. One of the most common of these purposes is the establishment of a dominance hierarchy. When certain types of animals are first placed in a common environment, the first thing they do is fight to assert their role in the dominance hierarchy. In general, the more dominant animals will be more aggressive than their subordinates.. The majority of conspecific aggression ceases about 24 hours after the introduction of the animals being tested.

There are many different theories that try to explain how males and females developed these different aggressive tendencies. One theory states that in species where one sex makes a higher parental investment than the other, the higher investing sex is a resource for which the other sex competes: in the majority of species, females are the higher investing sex. It also holds that the main objective of survival is to have the chance to pass on an individual’s genetic material. For males, it is of crucial importance to establish dominance and resource holding to obtain reproductive opportunities in order to pass on their genetics. Unlike females, whose reproductive success is constrained by long gestation and lactation periods, male reproductive success is constrained by the number of partners they can mate with. As a result, males employ physical aggression more often than females; they take more risks in order to compete with other males and gain an elevation of status. Males even go as far as killing one another and offspring belonging to other males. Males demonstrate less concern for their physical welfare in such competitions. In contrast, females compete with one another for resources, which can be converted to offspring. The establishment of dominance is more costly for females than for males and females have less to gain from achieving status. The female presence is more critical to the offspring’s survival and hence her reproductive success than is the father’s. It is only logical then that the health and well being of females would cause them to use less aggressive, low risk, and indirect strategies to acquire resources. As a result, in the majority of female-female conflicts, females rarely inflict serious damage to one another over resources. When translated to human, these facts suggest that women should be expected to show less evidence of dominance hierarchies than men do. In society, aggression in boys becomes increasingly motivated by issues of social status and self-esteem, which are usually decided by varying degrees of aggressive reactivity to personal challenge. Aggression in girls, focusing mainly on resource acquisition and not status, is more likely to take less physically dangerous and more covert forms of indirect aggression . There are, however, extensive critiques of the use of animal behavior to explain human behavior and the application of evolutionary explanations of contemporary human behavior while lesions of this area greatly reduce competitive drive and aggression(Bauman et al 2006). Several experiments in attack-primed Syrian Golden Hamsters support the claim of the amygdala being involved in control of aggression. Using expression of c-fos as a neuroanatomically localized marker of activity, the neural circuitry involved in the state of “attack readiness” in attack primed hamsters was studied. The results showed that certain structures of the amygdala were involved in aggressiveness: the medial nucleus and the cortical nuclei showed distinct differences in involvement as compared to other structures such as the lateral and basolateral nuclei and central nucleus of the amygdala, which were not associated with any substantial changes in aggressiveness. In addition, c-fos expression was found most clearly in the most dorsal and caudal aspects of the corticomedial amygdala (CMA). In the same study, it was also shown that lesions of the CMA significantly reduced the number of aggressive behaviors. Eight of eleven subjects failed to attack. Also a correlation between lesion site and attack latency was determined: the more anterior the lesion, the longer mean elapsed time to the aggressive behavior . Another area, the hypothalamus, is believed to serve a regulatory role in aggression. The hypothalamus has been shown to cause aggressive behavior when electrically stimulated and espresses receptors that help determine aggression levels based on their interactions with the neurotransmitters serotonin and vasopressin.

Another brain area associated with the regulation of aggression is the prefrontal cortex (PFC), which has been implicated in aggressive psychopathology. Reduced activity of the prefrontal cortex, in particular its medial and orbitofrontal portions, has been associated with violent/antisocial aggression. Specifically, regulation of the levels of the neurotransmitter serotonin in the PFC has been connected with a particular type of pathological aggression, induced by subjecting genetically predisposed, aggressive, wild-type mice to repeated winning experience; the male mice selected from aggressive lines had lower serotonin tissue levels in the PFC than the low-aggressive lines in this study .

Neurotransmitters and Hormones

Various neurotransmitters and hormones have been shown to correlate with aggressive behavior. The most often mentioned of these is the hormone testosterone. In one source, it was noted that concentration of testosterone most clearly correlated with aggressive responses involving provocation.ADD CITATION In adulthood, it is clear that testosterone is not related to any consistent methods of measuring aggression on personality scales,ADD CITATION but several studies of the concentration of blood testosterone of convicted male criminals who committed violent crimes compared to males without a criminal record or who committed non-aggressive crimes revealed in most cases that men who were judged aggressive/dominant had higher blood concentrations of testosterone than controls.ADD CITATION However, a correlation between testosterone levels and aggression does not prove a causal role for testosterone. Studies of testosterone levels of male athletes before and after a competition revealed that testosterone levels rise shortly before their matches, as if in anticipation of the competition, and are dependent on the outcome of the event: testosterone levels of winners are high relative to those of losers. Interestingly, testosterone levels in female criminals versus females without a criminal record mirror those of males: testosterone levels are higher in women who commit aggressive crimes or are deemed aggressive by their peers than non-aggressive females. However, no specific response of testosterone levels to competition was observed in female athletes, although a mood difference was noted. Testosterone has been shown to correlate with aggressive behavior in mice and in some humans, but in contrast to some long-standing theories, various experiments have failed to find a relationship between testosterone levels and aggression in humans. The possible correlation between testosterone and aggression could explain the "roid rage" that can result from anabolic steroid use, although an effect of abnormally high levels of steroids does not prove an effect at physiological levels.

Another line of research has focused more on the effects of circulating testosterone on the nervous system mediated by local metabolism within the brain. Testosterone can be metabolized to 17b-estradiol by the enzyme aromatase or to 5a-dihydrotestosterone by 5a-reductase. Aromatase is highly expressed in regions involved in the regulation of aggressive behavior, such as the amygdala and hypothalamus. In studies using genetic knock out techniques in inbred mice, male mice that lacked a functional aromatase enzyme displayed a marked reduction in aggression. Long-term treatment of these mice with estradiol partially restored aggressive behavior, suggesting that the neural conversion of circulating testosterone to estradiol and its effect on estrogen receptors affects inter-male aggression. Also, two different estrogen receptors, ERa and ERb, have been identified as having the ability to exert different effects on aggression. In studies using estrogen receptor knockout mice, individuals lacking a functional ERa displayed markedly reduced inter-male aggression while male mice that lacked a functional ERb exhibited normal or slightly elevated levels of aggressive behavior. These results imply that ERa facilitates male-male aggression, where as ERb may inhibit aggression. However, different strains of mice show the opposite pattern in that aromatase activity is negatively correlated with aggressive behavior. Also, in a different strain of mice the behavioral effect of estradiol is dependent on daylength: under long-days (16h of light) estradiol reduces aggression, and under short-days (8h of light) estradiol rapidly increases aggression .

Glucocorticoids also play an important role in regulating aggressive behavior. In adult rats, acute injections of corticosterone promote aggressive behavior and acute reduction of corticosterone decreases aggression; however, a chronic reduction of corticosterone levels can produce abnormally aggressive behavior. In addition, glucocorticoids affect development of aggression and establishment of social hierarchies. Adult mice with low baseline levels of corticosterone are more likely to become dominant than are mice with high baseline corticosterone levels .

Dehydroepiandrosterone (DHEA) is the most abundant circulating androgen and can be rapidly metabolized within target tissues into potent androgens and estrogens. Gonadal steroids generally regulate aggression during the breeding season, but non-gonadal steroids may regulate aggression during the non-breeding season. Castration of various species in the non-breeding season has no effect on territorial aggression. In several avian studies, circulating DHEA has been found to be elevated in birds during the non-breeding season. These data support the idea that non-breeding birds combine adrenal and/or gonadal DHEA synthesis with neural DHEA metabolism to maintain territorial behavior when gonadal testosterone secretion is low. Similar results have been found in studies involving different strains of rats, mice, and hamsters. DHEA levels also have been studied in humans and may play a role in human aggression. Circulating DHEAS (its sulfated ester) levels rise during adrenarche (~7 years of age) while plasma testosterone levels are relatively low. This implies that aggression in pre-pubertal children with aggressive conduct disorder might be correlated with plasma DHEAS rather than plasma testosterone, suggesting an important link between DHEAS and human aggressive behavior .

Another chemical messenger with implications for aggression is the neurotransmitter serotonin. In various experiments, serotonin action was shown to be negatively correlated with aggression(Delville et al. 1997). This correlation with aggression helps to explain the aggression-reducing effects of selective serotonin reuptake inhibitors such as fluoxetine (Delville et al. 1997), aka prozac.

While serotonin and testosterone have been the two most researched chemical messengers with regards to aggression, other neurotransmitters and hormones have been shown to relate to aggressive behavior as well. The neurotransmitter vasopressin causes an increase in aggressive behavior when present in large amounts in the anterior hypothalamus (Delville et al. 1997). The effects of norepinephrine, cortisol, and other neurotransmitters are still being studied.

Genetics and Aggression

In a nonmammilian example, the fruitless gene in D. melanogaster is a critical determinant for how fruit flies fight. Patterns of aggression can be switched, with males using female patterns of aggression or females using male patterns, by manipulating either the fruitless or transformer genes in the brain. Candidate genes for differentiating aggression between the sexes are the Sry (sex determining region Y) gene, located on the Y chromosome and the Sts (steroid sulfatase) gene. The Sts gene encodes the steroid sulfatase enzyme, which is pivotal in the regulation of neurosteroid biosynthesis. It is expressed in both sexes, is correlated with levels of aggression among male mice, and increases dramatically in females after parturition and during lactation, corresponding to the onset of maternal aggression.