期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 104, 期 35, 页码 14146-14150出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0704621104
关键词
GABA; synaptic plasticity
资金
- NINDS NIH HHS [R01 NS045625, NS045625, NS44185, R01 NS044185] Funding Source: Medline
Emotional arousal, linked to a surge of norepinephrine (NE) in the amygdala, leads to creation of stronger and longer-lasting memories. However, little is known about the synaptic mechanisms of such modulatory NE influences. Long-term potentiation (LTP) in auditory inputs to the lateral nucleus of the amygdala was recently linked to the acquisition of fear memory. Therefore we explored whether LTP induction at thalamo-amygdala projections, conveying the acoustic conditioned stimulus information to the amygdala during fear conditioning, is under adrenergic control. Using whole-cell recordings from amygdala slices, we show that NE suppresses GABAergic inhibition of projection neurons in the lateral amygdala and enables the induction of LTP at thalamo-amygdala synapses under conditions of intact GABA(A) receptor-mediated inhibition. Our data indicate that the NE effects on the efficacy of inhibition could result from a decrease in excitability of local circuit inter-neurons, without direct effects of NE on release machinery of the GABA-containing vesicles or the size of single-quanta postsynaptic GABA(A) receptor-mediated responses. Thus, adrenergic modulation of local interneurons may contribute to the formation of fear memory by gating LTP in the conditioned stimulus pathways.
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