ePoster

STRESS INDUCES OXYTOCIN-GΑI-DEPENDENT REMODELING OF ASTROCYTES TO SHAPE NEURONAL RESPONSE IN THE AMYGDALA

Valentin Grelot

Centre National de la Recherche Scientifique (CNRS)

FENS Forum 2026 (2026)

Barcelona, Spain

Board PS06-09PM-229

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Poster Board

PS06-09PM-229

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Abstract

Anticipated reactions to stressful situations are vital for the survival and well-being of organisms, and abnormal reactions results stress-related disorders. The neuropeptide oxytocin is a key modulator ensuring well-adapted stress responses. Oxytocin acts on both neurons and astrocytes, but the molecular and cellular mechanisms mediating stress response remain poorly understood. Here, we focus on the amygdala, a crucial hub that integrates and processes sensory information through oxytocin-dependent mechanisms. Using an acute stress paradigm in mice, genetic and pharmacological manipulations combined with proteomic, morphological, electrophysiological and behavioral approaches, we reveal that oxytocinergic modulation of the freezing response to stress is mediated by transient Gαi-dependent retraction of astrocytic processes, followed by enhanced neuronal sensitivity to extracellular potassium in the amygdala. Our findings elucidate a pivotal role for astrocytes morphology-dependent modulation of brain circuits that is requiredfor proper anticipated behavioral response to stressful situations.

Top: 3D reconstruction of an astrocyte with GFP labelling. On the left, the astrocyte shows significant complexity under normal conditions. On the right, the astrocyte shows a loss of complexity under stress conditions. Bottom: General diagram of the project. Under normal conditions, the astrocyte present at the synapses recaptures potassium ions in order to balance ionic homeostasis, and the neurons have basal postsynaptic currents. After stress, the astrocyte is no longer present at the synapse and can no longer recapture potassium ions. The neurons therefore have post-synaptic currents with a greater amplitude.

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