Abstract

Four lines of research are reviewed which investigated the role of the amygdala, ventromedial hypothalamus, bed nucleus of the stria terminalis, ventral hippocampus and the benzodiazepine receptor in predatory aggression and defense in the cat. The first two lines of research involved permanently increasing defensive response to threat either by repeatedly inducing subclinical seizure discharges in the ventral hippocampus and amygdala or by administering the benzodiazepine inverse agonist, anxiogenic compound FG-7142. In the third line of research, defensive response of cats was both transiently and lastingly reduced by high frequency stimulation of the basolateral amygdala. The fourth line of research examined the relationship between spontaneous cellular response to species-characteristic threat and individual differences in transmission of neural activity between the amygdala and ventromedial hypothalamus. Together, these studies point to the importance of the amygdalo-ventromedial hypothalamic pathway in defensive response to some, but not all conspecific threats. They also implicate other limbic pathways in the suppression of predatory aggressive responses. The amygdalo-bed nucleus of the stria terminalis pathway does not appear to be important in mediating defensive response to prey, but it is implicated in suppression of some types of predatory aggression. Neural inhibition and facilitation in particular cell fields of the ventral hippocampus seem to play a role in modulation of predatory aggression. Finally, the benzodiazepine receptor may be involved in modulating excitability in the amygdalo-VMH pathway, and it may also participate in a separate neural substrate which suppresses approach-attack behaviors.

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