Inhibition in the amygdala anxiety circuitry.
Inhibition in the amygdala anxiety circuitry.
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DOI：
10.1038/s12276-018-0063-8
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发表时间：
2018-04-09
影响因子：
12.8
通讯作者：
Krueger-Burg D
中科院分区：
文献类型：
--
作者：
Babaev O;Piletti Chatain C;Krueger-Burg D
抑制性神经传递在焦虑症中起着关键作用，苯二氮卓类γ-氨基丁酸受体激动剂的抗焦虑作用和最近在抑制性突触分子成分中发现的与焦虑相关的变体证明了这一点。因此，相当大的兴趣集中在了解抑制性神经元和突触如何对适应性和病理性焦虑行为背后的回路做出贡献。焦虑回路的一个关键元素是杏仁核，它整合了大脑皮层和丘脑感觉输入的信息，产生与恐惧和焦虑相关的行为输出。杏仁核内的信息处理严重依赖于抑制控制，尽管杏仁核GABA能神经元和突触调节焦虑相关行为的具体机制才刚刚开始被发现。在这里，我们总结了目前的知识状况，并强调了关于抑制在杏仁核焦虑回路中的作用的开放问题。我们讨论了在杏仁基底外侧核和中央杏仁核中参与焦虑信息处理的抑制性神经元亚型，以及在焦虑回路中形成抑制性突触传递的分子决定因素，如GABA受体和突触组织蛋白。最后，我们总结了当前和未来将这些知识转化为成功的焦虑症治疗策略的方法。了解杏仁核中的抑制性神经传递是开发更有效的抗焦虑疗法的关键。焦虑症是最常见的一组精神疾病，但由于目前治疗方法的疗效和耐受性有限，它们往往得不到足够的治疗。德国哥廷根马克斯·普朗克实验医学研究所的Dilja Krueger-Burg和他的同事回顾了目前关于杏仁核抑制神经元电路和分子机制的知识，这些神经回路和分子机制导致杏仁核的焦虑行为，杏仁核是处理情绪的关键大脑区域。众所周知，抑制性神经传递的改变和过度的兴奋性神经传递是焦虑症的基础。使用最新的技术来识别与调节焦虑相关行为有关的神经元群体和突触成分，应该有助于开发副作用更少的新的靶向治疗方法。
Inhibitory neurotransmission plays a key role in anxiety disorders, as evidenced by the anxiolytic effect of the benzodiazepine class of γ-aminobutyric acid (GABA) receptor agonists and the recent discovery of anxiety-associated variants in the molecular components of inhibitory synapses. Accordingly, substantial interest has focused on understanding how inhibitory neurons and synapses contribute to the circuitry underlying adaptive and pathological anxiety behaviors. A key element of the anxiety circuitry is the amygdala, which integrates information from cortical and thalamic sensory inputs to generate fear and anxiety-related behavioral outputs. Information processing within the amygdala is heavily dependent on inhibitory control, although the specific mechanisms by which amygdala GABAergic neurons and synapses regulate anxiety-related behaviors are only beginning to be uncovered. Here, we summarize the current state of knowledge and highlight open questions regarding the role of inhibition in the amygdala anxiety circuitry. We discuss the inhibitory neuron subtypes that contribute to the processing of anxiety information in the basolateral and central amygdala, as well as the molecular determinants, such as GABA receptors and synapse organizer proteins, that shape inhibitory synaptic transmission within the anxiety circuitry. Finally, we conclude with an overview of current and future approaches for converting this knowledge into successful treatment strategies for anxiety disorders. Understanding inhibitory neurotransmission in the amygdala is key to developing more effective therapeutics against anxiety. Anxiety disorders are the most prevalent group of psychiatric diseases, yet they are often under-treated due to the limited efficacy and tolerability of current treatment approaches. Dilja Krueger-Burg and colleagues at the Max Planck Institute of Experimental Medicine in Göttingen, Germany, review current knowledge of the inhibitory neuronal circuits and molecular mechanisms that contribute to anxiety behaviors in the amygdala, a key brain region for processing emotions. It is well established that alterations in inhibitory neurotransmission and excessive excitatory neurotransmission underlie anxiety disorders. Using the latest technologies to identify the neuronal populations and synaptic components implicated in the regulation of anxiety-related behaviors should help to develop new targeted treatments with fewer side-effects.
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DOI：
10.1002/syn.21953
发表时间：
2017-04
期刊：
Synapse (New York, N.Y.)
影响因子：
--
作者：
Calakos KC;Blackman D;Schulz AM;Bauer EP
通讯作者：
Bauer EP
影响因子：
13.9
作者：
Buzsáki G;Wang XJ
通讯作者：
Wang XJ
影响因子：
4.8
作者：
Dixon CL;Sah P;Keramidas A;Lynch JW;Durisic N
通讯作者：
Durisic N
影响因子：
2.4
作者：
Chandra, D;Korpi, ER;Homanics, GE
通讯作者：
Homanics, GE
影响因子：
2.5
作者：
Delaney, A. J.;Esmaeili, A.;Sah, P.
通讯作者：
Sah, P.