Department of Psychiatry and Psychotherapy, University Medical Center, Faculty of Medicine, University of Freiburg, Hauptstrasse 5, 79104 Freiburg, Germany; Department of Forensic Psychiatry, Institute of Forensic Medicine, University of Bern, Falkenplatz 18, 3012 Bern Switzerland.
Department of Psychiatry and Psychotherapy, University Medical Center, Faculty of Medicine, University of Freiburg, Hauptstrasse 5, 79104 Freiburg, Germany.
Neurosci Biobehav Rev. 2018 May;88:63-72. doi: 10.1016/j.neubiorev.2018.03.014. Epub 2018 Mar 14.
There is an urgent, unmet clinical need for faster and more efficient antidepressant drugs with higher response rates. In animal models of depression it was shown in the last few years that inhibition of three signaling molecules (BDNF, p11 and Homer1a) prevents efficacy of antidepressant therapy. These data not only show the crucial role of these factors for the treatment of depression, but may also point towards a better understanding of the molecular changes responsible for successful antidepressant therapy. Reviewing the literature concerning BNDF, p11 and Homer1a we here describe a molecular network in which these molecules interact with each other finally leading to facilitation of AMPA receptor signaling and plasticity, corroborating the current idea of AMPA receptors being a promising drug target in depression.
目前临床上急需起效更快、效率更高、应答率更高的抗抑郁药物。近年来，在抑郁症的动物模型中发现，抑制三种信号分子（BDNF、p11 和 Homer1a）会阻碍抗抑郁治疗的效果。这些数据不仅表明了这些因素对抑郁症治疗的关键作用，而且可能有助于更好地理解导致抗抑郁治疗成功的分子变化。在对 BDNF、p11 和 Homer1a 的文献进行综述后，我们在此描述了一个分子网络，其中这些分子相互作用，最终促进 AMPA 受体信号转导和可塑性，这印证了 AMPA 受体作为抗抑郁药物靶点的现有观点。
