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听觉恐惧条件反射促进外侧杏仁核到基底杏仁核突触的神经递质释放。

Auditory fear conditioning facilitates neurotransmitter release at lateral amygdala to basal amygdala synapses.

机构信息

Department of Life and Nanopharmaceutical Sciences, Kyung Hee University, Seoul, 02447, Republic of Korea.

Department of Biology, Kyung Hee University, Seoul, 02447, Republic of Korea.

出版信息

Biochem Biophys Res Commun. 2021 Dec 20;584:39-45. doi: 10.1016/j.bbrc.2021.11.014. Epub 2021 Nov 8.

DOI:10.1016/j.bbrc.2021.11.014
PMID:34768080
Abstract

The lateral amygdala (LA) is a main sensory input site from the cortical and thalamic regions. In turn, LA glutamatergic pyramidal neurons strongly project to the basal amygdala (BA). Although it is well known that auditory fear conditioning involves synaptic potentiation in the LA, it is not clear whether the LA-BA synaptic transmission is modified upon auditory fear conditioning. Here we found that high-frequency stimulation ex vivo resulted in long-term potentiation (LTP) with a concomitant enhancement of neurotransmitter release at LA-BA synapses. Auditory fear conditioning also led to the presynaptic facilitation at LA-BA synapses. Meanwhile, AMPA/NMDA current ratio was not changed upon fear conditioning, excluding the involvement of postsynaptic mechanism. Notably, fear conditioning occluded electrically induced ex vivo LTP in the LA-BA pathway, indicating that the conditioning and electrically induced LTP share common mechanisms. Our findings suggest that the presynaptic potentiation of LA-BA synapses may be involved in fear conditioning.

摘要

外侧杏仁核(LA)是皮质和丘脑区域的主要感觉输入部位。反过来,LA 谷氨酸能锥体神经元强烈投射到基底杏仁核(BA)。虽然众所周知听觉恐惧条件反射涉及 LA 中的突触增强,但尚不清楚听觉恐惧条件反射是否会改变 LA-BA 的突触传递。在这里,我们发现离体高频刺激导致长时程增强(LTP),同时增强 LA-BA 突触处神经递质的释放。听觉恐惧条件反射也导致 LA-BA 突触的突触前易化。同时,恐惧条件反射后 AMPA/NMDA 电流比没有变化,排除了突触后机制的参与。值得注意的是,恐惧条件反射阻断了 LA-BA 通路中电诱导的离体 LTP,表明条件反射和电诱导的 LTP 具有共同的机制。我们的发现表明,LA-BA 突触的突触前增强可能参与恐惧条件反射。

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Auditory fear conditioning facilitates neurotransmitter release at lateral amygdala to basal amygdala synapses.听觉恐惧条件反射促进外侧杏仁核到基底杏仁核突触的神经递质释放。
Biochem Biophys Res Commun. 2021 Dec 20;584:39-45. doi: 10.1016/j.bbrc.2021.11.014. Epub 2021 Nov 8.
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Ex vivo depotentiation of conditioning-induced potentiation at thalamic input synapses onto the lateral amygdala requires GluN2B-containing NMDA receptors.体外去敏化条件诱导的丘脑传入突触对侧杏仁核的增强作用需要包含 GluN2B 的 NMDA 受体。
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Extinction of cued fear memory involves a distinct form of depotentiation at cortical input synapses onto the lateral amygdala.线索恐惧记忆的消除涉及到外侧杏仁核皮质输入突触上一种独特的去敏形式。
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Fear conditioning occludes LTP-induced presynaptic enhancement of synaptic transmission in the cortical pathway to the lateral amygdala.恐惧条件作用会阻断长时程增强(LTP)诱导的、在通向杏仁核外侧核的皮质通路中突触传递的突触前增强。
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Presynaptic HCN channel activity is required for the expression of long-term potentiation at lateral amygdala to basal amygdala synapses.在外侧杏仁核到基底杏仁核突触处,长时程增强的表达需要突触前 HCN 通道活动。
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Postsynaptic BDNF signalling regulates long-term potentiation at thalamo-amygdala afferents.突触后 BDNF 信号调节丘脑-杏仁核传入的长时程增强。
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Convergent but temporally separated inputs to lateral amygdala neurons from the auditory thalamus and auditory cortex use different postsynaptic receptors: in vivo intracellular and extracellular recordings in fear conditioning pathways.来自听觉丘脑和听觉皮层的对杏仁核外侧神经元的汇聚但时间上分离的输入使用不同的突触后受体:恐惧条件反射通路中的体内细胞内和细胞外记录。
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