694. Amygdala circuit mechanisms modulating emotional memory strength and extinction

Abstract

Abstract Background Environmental cues present during threatening situations become linked to danger. When these cues are encountered again, they trigger retrieval of a fear memory via specialized neural circuits that produce internal fear states and initiate defensive behaviors. In brain areas such as the basolateral amygdala (BLA), these cue-evoked fear states are encoded in neural activity and decoded by anatomically distinct neuronal subpopulations that project to downstream effector regions. Aims & Objectives Astrocytes are abundant glial cells that closely interact with neurons and display dynamic Ca2+ signaling that can influence synaptic transmission and behavior. Emerging evidence links astrocytic Ca2+ activity to sensory processing, state regulation, and fear-related adaptations, yet how astrocytes shape fear memory coding, plasticity, and circuit output in the basolateral amygdala remains unknown. This presentation will address the role of astrocytes in fear and extinction. Method The presentation will show experiments utilizing in vivo chemogenetics, calcium imaging and single-unit electrophysiology to study astrocytes in fear and extinction, using the mouse as a model species. Results Using in vivo Ca2+ imaging together with causal manipulations of astrocyte activity, the presentation will show data demonstrating that BLA astrocytes track fear state and regulate fear memory retrieval and extinction. By integrating astrocyte perturbations with in vivo neuronal Ca2+ imaging and electrophysiological recordings in the BLA, the presentation will reveal that astrocytic Ca2+ signaling supports neuronal encoding of fear memories and their readout via a BLA–prefrontal circuit. Discussion & Conclusions These findings presented identify astrocytes as critical contributors to the formation and updating of fear-state neural representations, challenging strictly neurocentric models of amygdala-dependent adaptive behavior.