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首页> 外文期刊>Neuron >Functional inactivation of a fraction of excitatory synapses in mice deficient for the active zone protein bassoon.
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Functional inactivation of a fraction of excitatory synapses in mice deficient for the active zone protein bassoon.

机译:缺乏活性区蛋白巴松的小鼠中一部分兴奋性突触的功能失活。

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Mutant mice lacking the central region of the presynaptic active zone protein Bassoon were generated to establish the role of this protein in the assembly and function of active zones as sites of synaptic vesicle docking and fusion. Our data show that the loss of Bassoon causes a reduction in normal synaptic transmission, which can be attributed to the inactivation of a significant fraction of glutamatergic synapses. At these synapses, vesicles are clustered and docked in normal numbers but are unable to fuse. Phenotypically, the loss of Bassoon causes spontaneous epileptic seizures. These data show that Bassoon is not essential for synapse formation but plays an essential role in the regulated neurotransmitter release from a subset of glutamatergic synapses.
机译:缺少突触前活性区蛋白Bassoon中心区域的突变小鼠被产生,以确立该蛋白在活性区的组装和功能中的作用,作为突触小泡对接和融合的位点。我们的数据表明,巴松管的丧失导致正常突触传递减少,这可以归因于大部分谷氨酸能突触的失活。在这些突触处,囊泡以正常数量聚集并停靠,但无法融合。从表型上来说,巴松管的丧失会导致自发性癫痫发作。这些数据表明,巴松管对于突触形成不是必需的,但在谷氨酸能突触的子集的调节的神经递质释放中起重要作用。

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