Attack priming in female Syrian golden hamsters is associated with a c-fos-coupled process within the corticomedial amygdala.

Allowing a resident hamster a single "priming" attack on a conspecific induces a transient aggressive arousal as indicated by a reduction in the latency and increase in the probability of attack on a second intruder presented within the next 30 min. We present two lines of evidence identifying the corticomedial amygdala as an important locus mediating this effect. (1) Attack priming significantly increases the number of neurons expressing immunocytochemically identified Fos protein in the corticomedial amygdala, but not elsewhere. Pursuit and biting of an inanimate object does not induce corticomedial amygdala c-fos expression of the same pattern or magnitude. The corticomedial amygdala contribution to the priming effect involves more than a non-specific arousal, since corticomedial amygdala c-fos expression does not correlate with locomotor activity, a standard indicator of such arousal. (2) Radiofrequency lesions of the corticomedial amygdala reduce aggression, the greatest reduction occurring with the more anterior lesions. Other behaviors, including a priming-like locomotor practice effect in a running wheel, are unaffected by corticomedial amygdala lesions. These findings suggest that attack priming is an aggression-specific effect resulting from a Fos-coupled change within neural circuitry of which the corticomedial amygdala is a part. From a theoretical point of view, these experiments suggest a new approach to the analysis of the mechanisms underlying aggressive behavior and the persistence of aggressive arousal. We present a sketch of a quantitative neurobehavioral model which relates attack probability to neural activation within the corticomedial amygdala. From a methodological viewpoint, these experiments extend the utility of mapping c-fos expression as a technique for localizing endogenous, behavior-specific processes within the central nervous system.

Facilitation of muricide in rats by cholinergic stimulation of the lateral hypothalamus.

The effect of cholinergic stimulation of the lateral hypothalamus on muricide in rats was evaluated in two experiments. In Experiment 1, injections of the cholinergic agonist carbachol (5.0-20.0 micrograms) were found to facilitate muricide in rats that spontaneously killed mice. In Experiment 2, rats were induced to kill mice by food deprivation and then stimulated with carbachol (2.5-5.0 micrograms). Facilitation of muricide was found to be coincident with increased scores on a handling difficulty (irritability) scale for the majority of rats. These results suggest that facilitation of muricide by cholinergic stimulation of lateral hypothalamic areas may be related to increases in irritable aggression.