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Preclinical study demonstrates impaired DMN connectivity reduces social behavior through OFC PV interneurons, indicating neurobiological links to social dysfunction.
Social interactions are critical for mental health and are frequently disrupted in neuropsychiatric disorders. Clinical data suggest a link between dysfunction of the default mode network (DMN) and social impairment. To advance our understanding of the neurobiological mechanisms underlying social dysfunction, we back-translate these clinical findings into a preclinical setup, demonstrating that impaired DMN connectivity - achieved through activation of Parvalbumin interneurons in the orbitofrontal cortex (OFC) reduces normal social behaviour.
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Khatamsaz et al. (2026) studied this question.
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