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Neuropsychopharmacology ; 40(12): 2753-63, 2015 Nov.
Article in English | MEDLINE | ID: mdl-25936641

ABSTRACT

The canonical view on the central amygdala has evolved from a simple output station towards a highly organized microcircuitry, in which types of GABAergic neurons in centrolateral (CeL) and centromedial (CeM) subnuclei regulate fear expression and generalization. How these specific neuronal populations are connected to extra-amygdaloid target regions remains largely unknown. Here we show in mice that a subpopulation of GABAergic CeL and CeM neurons projects monosynaptically to brainstem neurons expressing neuropeptide S (NPS). The CeL neurons are PKCδ-negative and are activated during conditioned fear. During fear memory retrieval, the efficacy of this GABAergic influence on NPS neurons is enhanced. Moreover, a large proportion of these neurons (~50%) contain prodynorphin and somatostatin, two neuropeptides inhibiting NPS neurons. We conclude that CeL and CeM neurons inhibit NPS neurons in the brainstem by GABA release and that efficacy of this connection is strengthened upon fear memory retrieval. Thereby, this pathway provides a possible feedback mechanism between amygdala and brainstem routes involved in fear and stress coping.


Subject(s)
Brain Stem/cytology , Central Amygdaloid Nucleus/cytology , Fear/physiology , GABAergic Neurons/physiology , Mental Recall/physiology , Neural Pathways/physiology , Neuropeptides/metabolism , Animals , Brain Stem/drug effects , CREB-Binding Protein/metabolism , Cholera Toxin/metabolism , Conditioning, Classical/drug effects , DNA-Binding Proteins/metabolism , DNA-Binding Proteins/pharmacology , Dynorphins/pharmacology , Fear/drug effects , GABA Agents/pharmacology , Gene Expression Regulation/drug effects , Gene Expression Regulation/genetics , Mental Recall/drug effects , Mice , Mice, Inbred C57BL , Mice, Transgenic , Neuropeptides/genetics , Neurotransmitter Agents/pharmacology , Protein Kinase C-delta/metabolism , Synaptic Transmission/drug effects , Synaptic Transmission/genetics , Transcription Factors/metabolism , Transcription Factors/pharmacology
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