文献检索，用中文搜 PubMed

Suppr 超能文献

核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Nutt D J, Glue P, Lawson C

Reckitt and Colman Psychopharmacology Unit, School of Medical Sciences, University Walk, Bristol, England.

Prog Neuropsychopharmacol Biol Psychiatry. 1990;14(5):737-52. doi: 10.1016/0278-5846(90)90044-h.

Recent neurochemical investigations have enhanced our understanding of the anxiety disorders. Emphasis has been placed on dysfunction in central benzodiazepine, serotonergic and noradrenergic systems. 2. Changes in activity of endogenous ligands for the benzodiazepine receptor or in benzodiazepine receptor sensitivity appear to modulate anxiety. 3. There is evidence of serotonergic involvement in anxiety, in that serotonin agonists may increase anxiety, whilst drugs that reduce serotonin function are anxiolytic. 4. Noradrenergic dysfunction, especially that of alpha-2-adrenoceptors, provides the strongest etiological evidence in the development of anxiety. 5. A number of testable hypotheses can be generated from our present knowledge. As a result, new and more specific treatments may become apparent for the anxiety disorders.

最近的神经化学研究增进了我们对焦虑症的理解。研究重点在于中枢苯二氮䓬、血清素能和去甲肾上腺素能系统的功能障碍。2. 苯二氮䓬受体内源性配体活性的变化或苯二氮䓬受体敏感性的变化似乎可调节焦虑。3. 有证据表明血清素能参与焦虑，因为血清素激动剂可能会增加焦虑，而降低血清素功能的药物具有抗焦虑作用。4. 去甲肾上腺素能功能障碍，尤其是α-2-肾上腺素能受体的功能障碍，为焦虑症的发展提供了最有力的病因学证据。5. 根据我们目前的知识可以提出一些可检验的假设。因此，可能会出现针对焦虑症的新的、更具特异性的治疗方法。

Nutt D J, Glue P, Lawson C

Reckitt and Colman Psychopharmacology Unit, School of Medical Sciences, University Walk, Bristol, England.

Prog Neuropsychopharmacol Biol Psychiatry. 1990;14(5):737-52. doi: 10.1016/0278-5846(90)90044-h.

Recent neurochemical investigations have enhanced our understanding of the anxiety disorders. Emphasis has been placed on dysfunction in central benzodiazepine, serotonergic and noradrenergic systems. 2. Changes in activity of endogenous ligands for the benzodiazepine receptor or in benzodiazepine receptor sensitivity appear to modulate anxiety. 3. There is evidence of serotonergic involvement in anxiety, in that serotonin agonists may increase anxiety, whilst drugs that reduce serotonin function are anxiolytic. 4. Noradrenergic dysfunction, especially that of alpha-2-adrenoceptors, provides the strongest etiological evidence in the development of anxiety. 5. A number of testable hypotheses can be generated from our present knowledge. As a result, new and more specific treatments may become apparent for the anxiety disorders.

最近的神经化学研究增进了我们对焦虑症的理解。研究重点在于中枢苯二氮䓬、血清素能和去甲肾上腺素能系统的功能障碍。2. 苯二氮䓬受体内源性配体活性的变化或苯二氮䓬受体敏感性的变化似乎可调节焦虑。3. 有证据表明血清素能参与焦虑，因为血清素激动剂可能会增加焦虑，而降低血清素功能的药物具有抗焦虑作用。4. 去甲肾上腺素能功能障碍，尤其是α-2-肾上腺素能受体的功能障碍，为焦虑症的发展提供了最有力的病因学证据。5. 根据我们目前的知识可以提出一些可检验的假设。因此，可能会出现针对焦虑症的新的、更具特异性的治疗方法。