Brain Mechanisms of Aggressive Behavior; An Updated Review
Sensory Analyzers and Synthesizers for Motivating Stimuli:
Offense and Patrol/Marking
Page 11

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

As indicated in the model, both offense and patrol marking apparently share many of the same motivating stimulus inputs. In muroid rodents these inputs are largely chemosensory, including inputs from both the main olfactory bulb and the vomeronasal system whose inputs converge at several levels in the forebrain (Halpern and Martinez-Marcos, 2003).

The sensory analyzers of androgen-dependent pheromones in females and estrogen-dependent pheromones in males have a unique dual effect, each facilitating patrol/marking and sexual behavior and inhibiting offense. This may involve the ventral part of the premammillary nucleus which has shown to be active in the male in response to female odors (Yokosuka et al., 1999) and during sexual behavior (Kollack-Walker and Newman, 1995) and which apparently inhibits offense (Olivier et al, 1983; van den Berg et al., 1983).

The sensory analyzers of androgen-dependent pheromones in males should be located in a brain region where inputs are received from vomeronasal detection of androgen-dependent pheromones, and where neural activity is facilitated by androgens (i.e. offense that has been reduced by castration should be reinstated by injection of androgens at this point). Different results have been obtained in this regard from rats and mice. In rats androgens reinstate intermale offense in castrated males when injected into the medial preoptic area but not the septum (Bean and Conner, 1978). In mice androgens have this effect in the septum but not in the medial preoptic area (Lisciotto et al., 1990).

Detailed genetic analysis of offense elicited by androgen-dependent and non-androgen dependent pheromones may provide an experimental model that can be used to understand the brain mechanisms involved (Monahan and Maxson, 1998).

Another kind of behavioral plasticity is the priming effect for offense which apparently depends upon the corticomedial amygdala (Potegal et al., 1996a and 1996b). This is a temporary facilitation of offense lasting for minutes or, at most, hours after an attack. Although it is a temporary phenomenon and not technically a kind of learning, it has been added to the model within this framework (learning point 8). This may explain the results of an earlier study in which corticomedial amygdala lesions reduced offense in experienced but not inexperienced rats (Vochteloo and Koolhaas, 1987), a result that the authors attributed to an unidentified learning process.

Several earlier reports that 22 kHz ultrasonic cries may inhibit offense led to the proposal in my earlier review (Adams, 1979a) that they served as an inhibitory motivating stimulus of offense. An alternative view is presented by Blanchard et al. (1991) who suggest that the effect is mediated by defense; i.e. that 22 kHz ultrasound cries may evoke defense which, in turn, reduces offense. This is supported by the finding that similar ultrasonic signals produce defense (Mongeau et al., 2003). With this in mind, the model has been changed to indicate alarm calls as a facilitative motivating stimulus of defense rather than an inhibitory motivating stimulus of offense.

The neural basis of the motivating stimuli specific to competitive fighting have not been investigated in recent years, although earlier research, reviewed previously (Adams, 1979a), implicated the cortical amygdala, periamygdaloid cortex, and stria terminalis.

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