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Proximity in mice induced by an auditory-conditioned stimulus.

Wataru Ito¹, Alexei Morozov^2,3

¹Fralin Biomedical Research Institute Center for Neurobiology Research at Virginia Tech Carilion, Roanoke, VA, USA. wataru.ito@gmail.com.

Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology

|July 15, 2026

Summary

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Learned threats, like a conditioned stimulus (CS), can increase social proximity in mice. This effect requires familiarity and specific brain pathways, suggesting shared threat responses.

Area of Science:

Neuroscience
Behavioral Biology
Social Behavior

Background:

Social affiliation is crucial for survival and well-being.
Proximity to others is essential for social contact.
Innate threats increase social proximity, but learned threats' effects are unknown.

Purpose of the Study:

To investigate if learned threats, specifically an auditory conditioned stimulus (CS), induce social proximity in mice.
To identify the neural mechanisms and conditions underlying CS-evoked proximity.

Main Methods:

Fear conditioning in mice using an auditory CS.
Observing proximity in same-sex dyads during CS presentation.
Utilizing DREADD-mediated suppression to test the role of basolateral amygdala-to-ventral hippocampus pathways.

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Administering an oxytocin receptor antagonist (L368,899) to assess oxytocin signaling.

Main Results:

Fear-conditioned mice showed increased proximity during CS presentation, irrespective of freezing behavior.
CS-evoked proximity was dependent on partner familiarity.
Proximity required intact basolateral amygdala-to-ventral hippocampus connections.
Oxytocin receptor signaling was essential for this learned threat-induced proximity.

Conclusions:

Learned threats can elicit social proximity, similar to innate threats.
Shared neural circuitry, involving the amygdala-hippocampus pathway and oxytocin signaling, may underlie proximity responses to both learned and innate threats.
Familiarity plays a critical role in learned threat-induced social buffering.