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焦虑症:去甲肾上腺素能神经传递。

Anxiety disorders: noradrenergic neurotransmission.

作者信息

Neumeister A, Daher R J, Charney D S

机构信息

Mood and Anxiety Disorders Research Program, National Institute of Mental Health/NIH, 15K North Drive, MSC 2670, Bethesda MD, 20892-2670, USA.

出版信息

Handb Exp Pharmacol. 2005(169):205-23. doi: 10.1007/3-540-28082-0_8.

Abstract

The past decade has seen a rapid progression in our knowledge of the neurobiological basis of fear and anxiety. Specific neurochemical and neuropeptide systems have been demonstrated to play important roles in the behaviors associated with fear and anxiety-producing stimuli. Long-term dysregulation of these systems appears to contribute to the development of anxiety disorders, including panic disorder, posttraumatic stress disorder (PTSD), and social anxiety disorder. These neurochemical and neuropeptide systems have been shown to have effects on distinct cortical and subcortical brain areas that are relevant to the mediation of the symptoms associated with anxiety disorders. Moreover, advances in molecular genetics portend the identification of the genes that underlie the neurobiological disturbances that increase the vulnerability to anxiety disorders. This chapter reviews clinical research pertinent to the neurobiological basis of anxiety disorders. The implications of this synthesis for the discovery of anxiety disorder vulnerability genes and novel psychopharmacological approaches will also be discussed.

摘要

在过去十年中,我们对恐惧和焦虑的神经生物学基础的认识取得了迅速进展。特定的神经化学和神经肽系统已被证明在与恐惧和产生焦虑的刺激相关的行为中起重要作用。这些系统的长期失调似乎促成了焦虑症的发展,包括惊恐障碍、创伤后应激障碍(PTSD)和社交焦虑障碍。这些神经化学和神经肽系统已被证明对与焦虑症相关症状的介导相关的不同皮质和皮质下脑区有影响。此外,分子遗传学的进展预示着将识别出那些增加患焦虑症易感性的神经生物学紊乱背后的基因。本章回顾了与焦虑症神经生物学基础相关的临床研究。还将讨论这种综合研究对发现焦虑症易感性基因和新型心理药理学方法的意义。

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