Renger J J, Egles C, Liu G
RIKEN-MIT Neuroscience Research Center, Center for Learning and Memory, Department of Brain and Cognitive Sciences and, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Neuron. 2001 Feb;29(2):469-84. doi: 10.1016/s0896-6273(01)00219-7.
Formation of glutamatergic synapses entails development of "silent" immature contacts into mature functional synapses. To determine how this transformation occurs, we investigated the development of neurotransmission at single synapses in vitro. Maturation of presynaptic function, assayed with endocytotic markers, followed accumulation of synapsin I. During this period, synaptic transmission was primarily mediated by activation of NMDA receptors, suggesting that most synapses were functionally silent. However, local glutamate application to silent synapses indicated that these synapses contained functional AMPA receptors, suggesting a possible presynaptic locus for silent transmission. Interference with presynaptic vesicle fusion by exposure to tetanus toxin reverted functional to silent transmission, implicating SNARE-mediated fusion as a determinant of the ratio of NMDA:AMPA receptor activation. This work reveals that functional maturation of synaptic transmission involves transformation of presynaptic silent secretion into mature synaptic transmitter release.
谷氨酸能突触的形成需要将“沉默”的未成熟突触联系发展为成熟的功能性突触。为了确定这种转变是如何发生的，我们在体外研究了单个突触处神经传递的发育过程。用内吞标记物检测的突触前功能成熟，是跟随突触素I的积累而发生的。在此期间，突触传递主要由NMDA受体的激活介导，这表明大多数突触在功能上是沉默的。然而，向沉默突触局部施加谷氨酸表明，这些突触含有功能性AMPA受体，这表明沉默传递可能存在突触前位点。通过暴露于破伤风毒素干扰突触前囊泡融合，可使功能性传递恢复为沉默传递，这表明SNARE介导的融合是NMDA:AMPA受体激活比例的一个决定因素。这项工作揭示了突触传递的功能成熟涉及突触前沉默分泌向成熟突触递质释放的转变。
