Journal of Neuroscience
March 19, 2018
Katrin H. Preller, Leonhard Schilbach, Thomas Pokorny et al.
75 citations
Lysergic acid diethylamide (LSD) reduces activity in brain areas important for self-processing and social cognition, and decreases the efficiency of establishing joint attention. These effects are attributable to stimulation of the serotonin 2A receptor (5-HT2AR), as they are blocked by the antagonist ketanserin. The findings point toward the 5-HT2AR system as a potential target for treating social impairments in psychiatric disorders.
Philosophical transactions of the Royal Society of London. Series B, Biological sciences
February 13, 2023
Dimitris Bolis, Guillaume Dumas, Leonhard Schilbach
71 citations
Social interactions rely on interpersonal attunement, a multi-scale process of building and materializing social expectations. While common ground is cultivated through communication and culture, the mechanisms involved have often been studied in isolation. Collective psychophysiology can analyze social interactions without neglecting the individual. Mismatched expectations can break communication and lead to social isolation, negatively affecting mental health. Psychiatric disorders can be understood as disorders of social interaction, or interpersonal misattunement. This suggests an inter-personalized psychiatry that moves from a static disorder spectrum to a dynamic relational space, focusing on how social interaction promotes mental health.
medRxiv : the preprint server for health sciences
October 21, 2024
Pascal Grumbach, Jan Kasper, Joerg F Hipp et al.
1 citation
preprint
Autism spectrum disorder involves altered resting-state brain function, and an imbalance between excitation and inhibition is a proposed mechanism. In two large independent cohorts, individuals with autism consistently showed reduced local brain activity in default mode network nodes and increased activity in temporal regions, cerebellum, and brainstem. These activity changes spatially overlapped with multiple neurotransmitter systems, including dopamine, glutamate, GABA, and acetylcholine. The NMDA-antagonist ketamine, but not the GABA-potentiator midazolam, induced activity changes resembling those seen in autism, suggesting that pharmacologically shifting the excitation-inhibition balance can mimic autism-related brain alterations.