Asede, Douglas Bosch, Daniel Lüthi, Andreas Ferraguti, Francesco Ehrlich, Ingrid
Hertie Institute for Clinical Brain Research 2Werner Reichardt Centre for Integrative Neuroscience University of Tubingen, Otfried-Muller-Straße 25, 72076 Tubingen, Germany Graduate School of Neural and Behavioral Sciences, International Max Planck Research School, University of Tubingen, Osterbergstrasse 72074 Tubingen, Germany, Friedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, 4058 Basel, Switzerland, Department of Pharmacology, Innsbruck Medical University, Peter Mayr Straße 1a, 6020 Innsbruck, Austria.
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 behavioural 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 behaviours via their direct sensory inputs.
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