Role of glutamate δ-2 receptors in activity-dependent competition between heterologous afferent fibers
Role of glutamate δ-2 receptors in activity-dependent competition between heterologous afferent fibers
复制标题
谷氨酸δ-2受体在异源传入纤维之间的活性依赖性竞争中的作用
DOI：
10.1073/pnas.171098398
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发表时间：
2001
影响因子：
11.1
通讯作者：
P. Strata
中科院分区：
文献类型：
--
作者：
L. Morando;R. Cesa;Roberta Rasetti;Robin Harvey;P. Strata
调节大脑中详细结构的一个原则是，在建立突触连接方面，活跃的终端比不活跃的终端具有竞争优势。众所周知，这一原理适用于竞争共同靶域的单个神经元群体内的纤维。在这里，我们发现了一个额外的规则，当两个神经元群体竞争两个连续的领土时适用。小脑Purkinje细胞树突有两个不同的突触区域，其棘突由两个独立的兴奋性输入支配，即平行纤维(PFS)和攀升纤维(CFs)。谷氨酸δ-2受体通常只存在于对其神经支配重要的PF脊椎上。河豚毒素阻断活动后，在CF域形成大量新的脊椎，并主要由PFS支配；所有的脊椎，包括那些仍然受到CFs支配的脊椎，都带有δ-2受体。因此，在没有活动的情况下，PFS获得了相对于CFS的竞争优势。整个树枝成为一个具有与PFS相关的分子线索的统一区域。为了进入它们适当的领地并保持突触联系，CFS必须是活跃的，并在局部抑制竞争对手传入的线索。
A principle that regulates detailed architecture in the brain is that active terminals have a competitive advantage over less active terminals in establishing synaptic connections. This principle is known to apply to fibers within a single neuronal population competing for a common target domain. Here we uncover an additional rule that applies when two neuronal populations compete for two contiguous territories. The cerebellar Purkinje cell dendrites have two different synaptic domains with spines innervated by two separate excitatory inputs, parallel fibers (PFs) and climbing fibers (CFs). Glutamate δ-2 receptors are normally present only on the PF spines where they are important for their innervation. After block of activity by tetrodotoxin, numerous new spines form in the CF domain and become innervated mainly by PFs; all spines, including those still innervated by the CFs, bear δ-2 receptors. Thus, in the absence of activity, PFs gain a competitive advantage over CFs. The entire dendritic arbor becomes a uniform territory with the molecular cues associated with the PFs. To access their proper territory and maintain synaptic contacts, CFs must be active and locally repress the cues of the competitor afferents.
影响因子：
56.9
作者：
Huh, GS;Boulanger, LM;Shatz, CJ
通讯作者：
Shatz, CJ