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足部电击或电刺激引起的蓝斑激活会抑制杏仁核神经元。

Locus coeruleus activation by foot shock or electrical stimulation inhibits amygdala neurons.

作者信息

Chen F-J, Sara S J

机构信息

Neuromodulation, Neural Plasticity and Cognition, CNRS UMR 7102, Université Pierre et Marie Curie-Paris6, 9 Quai Saint-Bernard, Batiment B 5eme etage, Paris, France.

出版信息

Neuroscience. 2007 Jan 19;144(2):472-81. doi: 10.1016/j.neuroscience.2006.09.037. Epub 2006 Nov 9.

Abstract

The noradrenergic nucleus locus coeruleus (LC) has a direct projection to the basal lateral amygdala (BLA). Behavioral, lesion and pharmacological studies suggest that this pathway has an important role in mediating responses to emotional stimuli and in the formation of long term memory. The effect of LC activation on the activity of BLA neurons in vivo is not known. Therefore, in the present experiments, simultaneous extracellular unit recordings were made in the two regions while the anesthetized rat received electrical stimulation of the paw to simulate a real-life acute stressor, commonly used as an aversive reinforcer in conditioning experiments. All LC neurons exhibited a multiphasic excitatory response followed by prolonged inhibition. Responses of BLA cells were more heterogeneous, but predominantly inhibitory, with a release from inhibition during the refractory phase of LC. Direct electrical stimulation of the LC with a single pulse also elicited an inhibitory response in BLA. BLA response to both footshock and LC stimulation was partially blocked by the beta adrenergic receptor antagonist, timolol, infused into the BLA. These experiments are the first to report in vivo effects of activation of the noradrenergic system on neuronal activity in the BLA.

摘要

去甲肾上腺素能蓝斑核(LC)直接投射至基底外侧杏仁核(BLA)。行为学、损伤及药理学研究表明,该神经通路在介导对情绪刺激的反应及长期记忆形成中起重要作用。LC激活对BLA神经元在体活性的影响尚不清楚。因此,在本实验中,当麻醉大鼠接受足部电刺激以模拟现实生活中的急性应激源(在条件反射实验中常用作厌恶强化物)时,同时在这两个区域进行细胞外单位记录。所有LC神经元均表现出多相兴奋性反应,随后是长时间抑制。BLA细胞的反应更具异质性,但主要为抑制性,在LC的不应期有抑制解除。用单个脉冲直接电刺激LC也能在BLA中引发抑制性反应。注入BLA的β肾上腺素能受体拮抗剂噻吗洛尔可部分阻断BLA对足部电击和LC刺激的反应。这些实验首次报道了去甲肾上腺素能系统激活对BLA神经元活性的在体效应。

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