期刊
NEURON
卷 86, 期 2, 页码 541-554出版社
CELL PRESS
DOI: 10.1016/j.neuron.2015.03.008
关键词
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资金
- Werner Reichardt Centre for Integrative Neuroscience (CIN) at the University of Tubingen, an Excellence Cluster - Deutsche Forschungsgemeinschaft (DFG) [EXC 307]
- Hertie Foundation
- Brain and Behavior Research Foundation (NARSAD)
- Volkswagenstiftung
- Novartis Research Foundation
- Austrian Science Fund Fonds zur Forderung der wissenschaftlichen Forschung (FWF) [P-22969-B11]
- Network of European Neuroscience Schools (NENS) fellowship
- Austrian Science Fund (FWF) [P 22969] Funding Source: researchfish
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 GABA(B) 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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