The adolescent brain and age-related behavioral manifestations

An evolved module for fear elicitation and fear learning with 4 characteristics is proposed. (a) The fear module is preferentially activated in aversive contexts by stimuli that are fear relevant in an evolutionary perspective. (b) Its activation to such stimuli is automatic. (c) It is relatively impenetrable to cognitive control. (d) It originates in a dedicated neural circuitry, centered on the amygdala. Evidence supporting these propositions is reviewed from conditioning studies, both in humans and in monkeys; illusory correlation studies; studies using unreportable stimuli; and studies from animal neuroscience. The fear module is assumed to mediate an emotional level of fear learning that is relatively independent and dissociable from cognitive learning of stimulus relationships.

Fears, phobias and preparedness: Toward an evolved module of fear and fear learning

The role of childhood trauma in the neurobiology of mood and anxiety disorders: preclinical and clinical studies

Empathy accounts for the naturally occurring subjective experience of similarity between the feelings expressed by self and others without loosing sight of whose feelings belong to whom. Empathy involves not only the affective experience of the other person’s actual or inferred emotional state but also some minimal recognition and understanding of another’s emotional state. In light of multiple levels of analysis ranging from developmental psychology, social psychology, cognitive neuroscience, and clinical neuropsychology, this article proposes a model of empathy that involves parallel and distributed processing in a number of dissociable computational mechanisms. Shared neural representations, self-awareness, mental flexibility, and emotion regulation constitute the basic macrocomponents of empathy, which are underpinned by specific neural systems. This functional model may be used to make specific predictions about the various empathy deficits that can be encountered in different forms of social and neu...

The functional architecture of human empathy

The ability to cognitively regulate emotional responses to aversive events is important for mental and physical health. Little is known, however, about neural bases of the cognitive control of emotion. The present study employed functional magnetic resonance imaging to examine the neural systems used to reappraise highly negative scenes in unemotional terms. Reappraisal of highly negative scenes reduced subjective experience of negative affect. Neural correlates of reappraisal were increased activation of the lateral and medial prefrontal regions and decreased activation of the amygdala and medial orbito-frontal cortex. These findings support the hypothesis that prefrontal cortex is involved in constructing reappraisal strategies that can modulate activity in multiple emotion-processing systems.

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Rethinking Feelings: An fMRI Study of the Cognitive Regulation of Emotion

Emotion is normally regulated in the human brain by a complex circuit consisting of the orbital frontal cortex, amygdala, anterior cingulate cortex, and several other interconnected regions. There are both genetic and environmental contributions to the structure and function of this circuitry. We posit that impulsive aggression and violence arise as a consequence of faulty emotion regulation. Indeed, the prefrontal cortex receives a major serotonergic projection, which is dysfunctional in individuals who show impulsive violence. Individuals vulnerable to faulty regulation of negative emotion are at risk for violence and aggression. Research on the neural circuitry of emotion regulation suggests new avenues of intervention for such at-risk populations.

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Dysfunction in the Neural Circuitry of Emotion Regulation--A Possible Prelude to Violence

Depression is a disorder of the representation and regulation of mood and emotion. The circuitry underlying the representation and regulation of normal emotion and mood is reviewed, including studies at the animal level, human lesion studies, and human brain imaging studies. This corpus of data is used to construct a model of the ways in which affect can become disordered in depression. Research on the prefrontal cortex, anterior cingulate, hippocampus, and amygdala is reviewed and abnormalities in the structure and function of these different regions in depression is considered. The review concludes with proposals for the specific types of processing abnormalities that result from dysfunctions in different parts of this circuitry and offers suggestions for the major themes upon which future research in this area should be focused.

Katherine M. Putnam

Papers

Dysfunction in the Neural Circuitry of Emotion Regulation--A Possible Prelude to Violence

Depression: perspectives from affective neuroscience.

Regional brain function, emotion and disorders of emotion.

Event-related functional magnetic resonance imaging measures of neural activity to positive social stimuli in pre- and post-treatment depression.

Normative emotion-modulated startle response in individuals at risk for schizophrenia–spectrum disorders