Goda Y, Stevens C F
Molecular Neurobiology Laboratory, Salk Institute La Jolla, California 92037, USA.
Neuron. 1996 Jan;16(1):103-11. doi: 10.1016/s0896-6273(00)80027-6.
Long-term depression (LTD) in pairs of cultured rodent hippocampal neurons was examined to study the molecular basis of this form of synaptic plasticity. We have previously characterized two components of transmitter release: a synchronous, fast phase that requires synaptotagmin I, and an asynchronous, slow component that persists in the absence of synaptotagmin I. Are these two release components differentially affected by the presynaptic changes of LTD, or is the mechanism of plasticity common to both? We find that LTD is expressed as parallel changes in the fast and slow components of release, and that this form of synaptic plasticity is still seen in the absence of functional synaptotagmin I. Any alterations in the presynaptic release machinery observed during LTD thus involve mechanisms shared by both modes of release.
为了研究这种形式的突触可塑性的分子基础，对培养的成对啮齿动物海马神经元中的长时程抑制（LTD）进行了检测。我们之前已经对递质释放的两个成分进行了表征：一个是同步的快速相，它需要突触结合蛋白I；另一个是异步的慢成分，在没有突触结合蛋白I的情况下仍然存在。这两个释放成分是否受到LTD突触前变化的不同影响，或者可塑性机制对两者来说是共同的？我们发现LTD表现为释放的快速和慢成分的平行变化，并且在没有功能性突触结合蛋白I的情况下仍然可以看到这种形式的突触可塑性。因此，在LTD期间观察到的突触前释放机制的任何改变都涉及两种释放模式共有的机制。
