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.

对于具有更高响应率的更快，更有效的抗抑郁药，迫切需要满足临床需求。在抑郁症的动物模型中，最近几年表明抑制三种信号分子（BDNF，p11和Homer1a）会阻止抗抑郁药治疗的功效。这些数据不仅显示了这些因素在抑郁症治疗中的关键作用，而且还可能指向更好地理解成功进行抗抑郁治疗的分子变化。在回顾有关BNDF，p11和Homer1a的文献时，我们在这里描述了一个分子网络，其中这些分子彼此相互作用，最终促进了AMPA受体信号传导和可塑性，从而证实了AMPA受体目前是抑郁症中有希望的药物靶点的想法。