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Observations from human subjects with focal brain lesions and animal subjects with experimental lesions have implicated a variety of brain regions in the mediation of social behavior. Previous studies carried out in the macaque monkey found that lesions of the amygdala not only decrease emotional reactivity but also disrupt normal social interactions. We have re-investigated the relationship between amygdala lesions and social behavior in cohorts of mature and neonatal rhesus monkeys who were prepared with selective and complete bilateral ibotenic acid lesions of the amygdaloid complex. These animals display clear alterations in emotional and social behavior. We interpret these changes as due to a loss of the ability to evaluate environmental stimuli as potential threats. However, adult animals with bilateral lesions of the amygdala demonstrate near normal, and even increased, social interactions with conspecifics. Moreover, neonatal animals, prepared with amygdala lesions at 2 weeks of age, also demonstrate species typical social behaviors such as the generation of facial expressions, grooming and play behavior. These results argue against the idea that the amygdala is essential for the interpretation of social communication or for the expression of social behavior. Because it does appear to participate in the evaluation of the "safety" of social interactions, we believe that it does have a role in modulating the amount of social behavior in which an organism will participate. However, our current answer to the question posed in the title of this paper is no!

Chronic stress facilitates fear conditioning in rats with hippocampal neuronal atrophy and in rats in which the atrophy is prevented with tianeptine, a serotonin re-uptake enhancer. The purpose of this study was to determine whether the lack of dissociation between fear conditioning performance and hippocampal integrity was masked by the presence of endogenous corticosteroids during training. As in previous studies, rats were stressed by daily restraint (6 h/day for 21 days), trained in the conditioning chamber (day 23), and then assessed for conditioned fear (day 25) at a time when hippocampal dendritic atrophy persists. On the training day, half of the control and stressed rats were injected with metyrapone to reduce corticosterone release. Two hours later, two paired or unpaired presentations of tone and footshock were delivered. Although metyrapone reduced conditioned fear in all rats, only stressed rats showed dissociated fear conditioning (i.e. tone conditioning was reduced while contextual conditioning was eliminated). Chronically stressed rats, regardless of metyrapone treatment displayed more rearing in the open field when tested immediately after the completion of fear conditioning. These data support the hypothesis that increased emotionality and enhanced fear conditioning exhibited by chronically stressed rats may be due to endogenous corticosterone secretion at the time of fear conditioned training. Moreover, these data suggest that chronic stress impairs hippocampal-dependent processes more robustly than hippocampal-independent processes after metyrapone to reduce corticosterone secretion during aversive training.

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