Brain Mechanisms of Aggressive Behavior; An Updated Review
Sensory Analyzers and Synthesizers for Motivating Stimuli:
Page 14

Title page & Abstract
Page 1

Page 2

Page 3

Behavioral Descriptions
Page 4

Motivational Mechanisms
Page 5

Defense Motivational Mechanism
Pages 6-7

Offense Motivational Mechanism
Page 8

Interactions &
Hormone Effects

Page 9

Relations in Hypothalamus
Page 10

Sensory Analyzers of Offense & Patrol/Marking
Page 11

Sensory Analyzers of Familiarity
Page 12

Sensory Analyzers of Defense
Pages 13-14

Motor Patterning Mechanisms
Page 15

Sensory Analyzers for Releasing & Directing Stimuli
Page 16

Testing the Model
Page 17

Acknowledgements & References
Pages 18-19-20-21-22-23-24-25

(continued from previous page)

The proposed consociate modulator may also be responsible for the differences in defensiveness between wild and domesticated animals. Wild animals, e.g. rats (Blanchard et al., 1994) and mice (Blanchard et al., 1998), show higher levels of defense in response to the full range of motivating stimuli and a particularly high level of lunge-and-bite attack. It is assumed that the consociate modulator would be more active in domesticated and laboratory animals as a result of their selective breeding against defensiveness and their association during upbringing with humans and other animals, and this would reduce their overall level of defense and, especially, the lunge-and-bite attack. As one would predict from this analysis, amygdala lesions tame wild cats (Ursin, 1965) and wild rats (Kemble et al., 1984), while not affecting defensive behavior of domestic cats (Ursin, 1965) or laboratory rats on hyperreactivey tests (Blanchard et al., 1979). Furthermore, septal lesions, which make domestic cats hyperdefensive, have no noticeable difference on wild cats (Ursin et al., 1981). One would predict that septal lesions which render laboratory rats hyperdefensive, should have no noticeable affect on the defensiveness of wild rats, but I am not aware of published data on the question.

Domesticated animals have been found to have higher brain levels of serotonin than wild animals (Hammer et al., 1990; Popova et al., 1991). Although serotonin affects structures throughout much of the forebrain, it originates for the most part from the nerve endings of a restricted number of localized neurons in the raphe nuclei of the midbrain. Neurons in the dorsal raphe nucleus in the tree shrew increase their activity during defense against the experimenter and against an attacking conspecific but not during offense behavior (Walletschek and Raab, 1982), although it is not known whether the neurons in question were serotonergic. Activity of the raphe nuclei are also shown to be active following defense according to c-Fos measures (Martinez et al., 1998). Although many effects of serotonin on defense are difficult to interpret, at least one finding is clear: it reduces anti-predator defense in wild rats (Blanchard et al., 1998). In the long term, the stress of repeated defeat elevates forebrain levels of serotonin (Blanchard et al., 1998), which may help shift the behavior of an animal away from active defense (anti-predator) and toward submission (exclusively consociate defense). Both the possible roles of serotonin in the process of domestication and in shifting an animal from anti-predator to consociate defense can be explained as a long term facilitative effect on the proposed consociate modulator. A similar effect was proposed previously for the corticosteroids that are secreted during defense (Adams, 1983).

There are reports that serotonin reduces offense as well as defense. In hamsters, serotonin reduces offense behavior, an effect apparently exerted on neurons of the anterior hypothalamus (offense motivational mechanism?) according to data obtained by Ferris et al (1997). Depletion of forebrain serotonin has been found to increase offense in male rats (Vergnes et al., 1988), and intraventricular administration of serotonin decreases offense in male but not female hamsters (Joppa et al., 1997).

previous page
home page
next page