Groth Rachel D, Tsien Richard W
Department of Molecular and Cellular Physiology, Stanford University, Stanford, CA 94305, USA.
Neuron. 2008 Oct 23;60(2):192-4. doi: 10.1016/j.neuron.2008.10.003.
Prolonged changes in neuronal activity trigger compensatory modifications in synaptic function to restore firing rates to normal levels. In this issue of Neuron, Aoto et al. demonstrate that synthesis of retinoic acid offsets chronic network inactivity by increasing synaptic strength through upregulation of GluR1 receptors.
神经元活动的长期变化会触发突触功能的代偿性改变,以使 firing 率恢复到正常水平。在本期《神经元》杂志中,Aoto 等人证明,视黄酸的合成通过上调 GluR1 受体来增加突触强度,从而抵消慢性网络不活动的影响。