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Updated: Apr 15, 2026

Ex Vivo Optogenetic Dissection of Fear Circuits in Brain Slices
Published on: April 5, 2016
Sensory inputs to intercalated cells provide fear-learning modulated inhibition to the basolateral amygdala
Douglas Asede1, Daniel Bosch2, Andreas Lüthi3
1Hertie Institute for Clinical Brain Research, University of Tübingen, Otfried-Müller-Straße 25, 72076 Tübingen, Germany; Werner Reichardt Centre for Integrative Neuroscience, University of Tübingen, Otfried-Müller-Straße 25, 72076 Tübingen, Germany; Graduate School of Neural and Behavioral Sciences, International Max Planck Research School, University of Tübingen, Österbergstrasse 3, 72074 Tübingen, Germany.
Abstract:
Increasing evidence suggests that parallel plastic processes in the amygdala involve inhibitory elements to control fear and extinction memory. GABAergic medial paracapsular intercalated cells (mpITCs) are thought to relay activity from basolateral nucleus (BLA) and prefrontal cortex to inhibit central amygdala output during suppression of fear. Recently, projection diversity and differential behavioral activation of mpITCs in distinct fear states suggest additional functions. Here, we show that mpITCs receive convergent sensory thalamic and cortical inputs that undergo fear learning-related changes and are dynamically modulated via presynaptic GABAB receptors recruited by GABA released from the mpITC network. Among mpITCs, we identify cells that inhibit but are also mutually activated by BLA principal neurons. Thus, mpITCs take part in fear learning-modulated feedforward and feedback inhibitory circuits to simultaneously control amygdala input and output nuclei. Our findings place mpITCs in a unique position to gate acquired amygdala-dependent behaviors via their direct sensory inputs.
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