Synapsin utilization differs among functional classes of synapses on thalamocortical cells
Synapsin utilization differs among functional classes of synapses on thalamocortical cells
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DOI：
10.1523/jneurosci.4631-05.2006
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发表时间：
2006-05-24
影响因子：
5.3
通讯作者：
Heggelund, Paul
中科院分区：
文献类型：
--
作者：
Kielland, Anders;Erisir, Alev;Heggelund, Paul
神经末梢中的几种蛋白质参与神经元之间的突触传递。突触蛋白是突触小泡相关蛋白，在大脑中广泛分布，并且被认为对于高速率突触传递过程中小泡的持续募集至关重要。我们比较了小鼠背外侧膝状核丘脑皮质细胞上两种谷氨酸能突触中突触蛋白的作用：视网膜原化突触，以高频传递初级传入输入并显示突触抑制；皮质原化突触，以较低频率提供调节反馈并显示突触促进。我们使用电生理学方法来确定突触蛋白 I 和 II 的基因敲除对配对脉冲、脉冲序列和强直后增强范式中短期突触可塑性的影响。基因失活改变了皮质原突触的可塑性，但没有改变视网膜原突触的可塑性。在野生型小鼠中使用针对突触蛋白的抗体进行的免疫染色表明，突触蛋白 I 和 II 均未出现在视黄质蛋白末端，而两者均出现在皮质原蛋白末端。在 GABA 能终端中，仅出现突触蛋白 I。在敲除小鼠的皮质末端中，突触小泡的密度降低，因为末端尺寸增加，而不是囊泡数量减少，并且与野生型小鼠相比，囊泡间距增加。在视黄质末端，敲除小鼠和野生型小鼠之间没有发生显着的形态差异。总之，这表明突触蛋白 I 和 II 不存在于视黄质末端，因此对于持续、高速率的突触传递不是必需的。
Several proteins in nerve terminals participate in synaptic transmission between neurons. The synapsins, which are synaptic vesicle-associated proteins, have widespread distribution in the brain and are assumed essential for sustained recruitment of vesicles during high rates of synaptic transmission. We compared the role of synapsins in two types of glutamatergic synapses on thalamocortical cells in the dorsal lateral geniculate nucleus of mice: retinogeniculate synapses, which transmit primary afferent input at high frequencies and show synaptic depression, and corticogeniculate synapses, which provide modulatory feedback at lower frequencies and show synaptic facilitation. We used electrophysiological methods to determine effects of gene knock-out of synapsin I and II on short-term synaptic plasticity in paired-pulse, pulse-train, and posttetanic potentiation paradigms. The gene inactivation changed the plasticity properties in corticogeniculate, but not in retinogeniculate, synapses. Immunostaining with antibodies against synapsins in wild-type mice demonstrated that neither synapsin I nor II occurred in retinogeniculate terminals, whereas both occurred in corticogeniculate terminals. In GABAergic terminals, only synapsin I occurred. In corticogeniculate terminals of knock-out mice, the density of synaptic vesicles was reduced because of increased terminal size rather than reduced number of vesicles and the intervesicle distance was increased compared with wild-type mice. In the retinogeniculate terminals, no significant morphometric differences occurred between knock-out and wildtype mice. Together, this indicates that synapsin I and II are not present in the retinogeniculate terminals and therefore are not essential for sustained, high-rate synaptic transmission.