Social interaction is a complex behavior which requires the individual to integrate various internal processes, such as social motivation, social recognition, salience, reward, and emotional state, as well as external cues informing the individual of others’ behavior, emotional state and social rank. This complex phenotype is susceptible to disruption in humans affected by neurodevelopmental and psychiatric disorders, including autism spectrum disorder (ASD). Multiple pieces of convergent evidence collected from studies of humans and rodents suggest that the prefrontal cortex (PFC) plays a pivotal role in social interactions, serving as a hub for motivation, affiliation, empathy, and social hierarchy. Indeed, disruption of the PFC circuitry results in social behavior deficits symptomatic of ASD. Here, we review this evidence and describe various ethologically relevant social behavior tasks which could be employed with rodent models to study the role of the PFC in social interactions. We also discuss the evidence linking the PFC to pathologies associated with ASD. Finally, we address specific questions regarding mechanisms employed by the PFC circuitry that may result in atypical social interactions in rodent models, which future studies should address.
Smith and Lane have suggested a model of emotion processing with at least three stations: areas like the amygdala, which process discrete body features areas like the anterior insula, which process whole-body patterns and areas like the medial prefrontal cortex, which process emotion concepts. Ben Shalom and Bonneh have suggested a model of the prefrontal cortex, in which medial BA 9 integrates emotional states, and lateral BA 9 performs selection/inhibition on these states. Taken together, the current paper suggests a pathway for emotion processing with at least four stations: areas like the amygdala, which process discrete body features areas like the anterior insula, which process whole-body patterns, medial BA 9 which integrates emotion concepts, and lateral BA 9, which performs selection/inhibition on these concepts. Following the existing literature, it then suggest that there is a significant involvement of the amygdala in psychopathy (Blair), of the anterior insula in alexithymia (Bird), of the medial BA 9 in deficits in somatosensory discrimination (Ben Shalom), and of lateral BA 9 in emotional impulsivity (Ronel).
Frontal lobe function may not universally explain all forms of attention deficit hyperactivity disorder (ADHD) but the frontal lobe hypothesis described supports an internally consistent model for integrating the numerous behaviors associated with ADHD. The paper examines the developmental trajectories of frontal and prefrontal lobe development, framing ADHD as maturational dysregulation concluding that the cognitive, motor, and behavioral abilities of the presumptive majority of ADHD children may not primarily be disordered or dysfunctional but reflect maturational dysregulation that is inconsistent with the psychomotor and cognitive expectations for the child’s chronological and mental age. ADHD children demonstrate decreased activation of the right and middle prefrontal cortex. Prefrontal and frontal lobe regions have an exuberant network of shared pathways with the diencephalic region, also having a regulatory function in arousal as well as with the ascending reticular formation which has a capacity for response suppression to task-irrelevant stimuli. Prefrontal lesions oftentimes are associated with the regulatory breakdown of goal-directed activity and impulsivity. In conclusion, a presumptive majority of childhood ADHD may result from maturational dysregulation of the frontal lobes with effects on the direct, indirect and/or, hyperdirect pathways.