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Updated: Apr 26, 2026

Continuous Theta Burst Stimulation of the Posterior Medial Frontal Cortex to Experimentally Reduce Ideological Threat Responses
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Orbitofrontal PV interneurons modulate social interaction via default mode network dynamics.

Elmira Khatamsaz1, Tudor M Ionescu1, Katja Keppler1

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|April 24, 2026
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Summary
This summary is machine-generated.

Impaired default mode network (DMN) connectivity, specifically in the orbitofrontal cortex (OFC), reduces social behavior in preclinical models. Activating Parvalbumin interneurons in the OFC disrupts DMN function and social interaction.

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Area of Science:

  • Neuroscience
  • Behavioral Science
  • Psychiatry

Background:

  • Social interactions are vital for mental health.
  • Neuropsychiatric disorders often involve social deficits.
  • Dysfunction in the default mode network (DMN) is linked to social impairment.

Purpose of the Study:

  • To investigate the neurobiological basis of social dysfunction.
  • To back-translate clinical observations of DMN dysfunction and social impairment into a preclinical model.
  • To understand how default mode network (DMN) connectivity impacts social behavior.

Main Methods:

  • Utilized a preclinical model to study social behavior.
  • Manipulated default mode network (DMN) connectivity via Parvalbumin interneuron activation in the orbitofrontal cortex (OFC).
  • Assessed the impact of altered DMN connectivity on social interactions.

Main Results:

  • Activation of Parvalbumin interneurons in the orbitofrontal cortex (OFC) impaired default mode network (DMN) connectivity.
  • This impairment in DMN connectivity led to a reduction in normal social behavior.
  • Demonstrated a causal link between specific DMN dysfunction and social deficits.

Conclusions:

  • Default mode network (DMN) connectivity is crucial for normal social behavior.
  • Orbitofrontal cortex (OFC) Parvalbumin interneurons play a role in regulating DMN function and social interaction.
  • Findings provide a neurobiological framework for understanding social impairments in neuropsychiatric disorders.