Amygdala is an intensively researched brain structure involved in social processing and multiple major clinical disorders, but its functions are not well understood. The functions of a brain structure are best hypothesized on the basis of neuroanatomical connectivity findings, and of behavioral, neuroimaging, neuropsychological and physiological findings. Among the heaviest neuroanatomical interconnections of amygdala are those with perirhinal cortex (PRC), but these are little considered in the theoretical literature. PRC integrates complex, multimodal, meaningful and fine-grained distributed representations of objects and (...) conspecifics. Consistent with this connectivity, amygdala is hypothesized to contribute meaningful and fine-grained representations of intangible knowledge for integration by PRC. Behavioral, neuroimaging, neuropsychological and physiological findings further support amygdala mediation of a diversity of such representations. These representations include subjective valence, impact, economic value, noxiousness, importance, ingroup membership, social status, popularity, trustworthiness and moral features. Further, the formation of amygdala representations is little understood, and is proposed to be often implemented through embodied cognition mechanisms. The hypothesis builds on earlier work, and makes multiple novel contributions to the literature. It highlights intangible knowledge, which is an influential but insufficiently researched factor in social and other behaviors. It contributes to understanding the heavy but neglected amygdala-PRC interconnections, and the diversity of amygdala-mediated intangible knowledge representations. Amygdala is a social brain region, but it does not represent species-typical social behaviors. A novel proposal to clarify its role is postulated. The hypothesis is also suggested to illuminate amygdala’s involvement in several core symptoms of autism spectrum disorder (ASD). Specifically, novel and testable explanations are proposed for the ASD symptoms of disorganized visual scanpaths, apparent social disinterest, preference for concrete cognition, aspects of the disorder’s heterogeneity, and impairment in some activities of daily living. Together, the presented hypothesis demonstrates substantial explanatory potential in the neuroscience, social and clinical domains. (shrink)

Early life adversity, such as child maltreatment or child poverty, engenders problems with emotional and behavioral regulation. In the quest to understand the neurobiological sequelae and mechanisms of risk, the amygdala has been of major focus. While the basic functions of this region make it a strong candidate for understanding the multiple mental health issues common after ELA, extant literature is marked by profound inconsistencies, with reports of larger, smaller, and no differences in regional volumes of this area. We believe (...) integrative models of stress neurodevelopment, grounded in “allostatic load,” will help resolve inconsistencies in the impact of ELA on the amygdala. In this review, we attempt to connect past research studies to new findings with animal models of cellular and neurotransmitter mediators of stress buffering to extreme fear generalization onto testable research and clinical concepts. Drawing on the greater impact of inescapability over unpredictability in animal models, we propose a mechanism by which ELA aggravates an exhaustive cycle of amygdala expansion and subsequent toxic-metabolic damage. We connect this neurobiological sequela to psychosocial mal/adaptation after ELA, bridging to behavioral studies of attachment, emotion processing, and social functioning. Lastly, we conclude this review by proposing a multitude of future directions in preclinical work and studies of humans that suffered ELA. (shrink)