The spatial organization of long-term synaptic plasticity at the input stage of cerebellum
The spatial organization of long-term synaptic plasticity at the input stage of cerebellum
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DOI：
10.1523/jneurosci.4873-06.2007
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发表时间：
2007-02-07
影响因子：
5.3
通讯作者：
D'Angelo, Egidio
中科院分区：
文献类型：
--
作者：
Mapelli, Jonathan;D'Angelo, Egidio
长期突触可塑性[长期增强（LTP）和长期抑制（LTD）]的空间组织被认为在神经元网络中的分布式信号处理中发挥着关键作用，但其性质在大多数中央回路中仍未确定。通过使用多电极阵列记录，我们重建了小脑切片中颗粒层的激活图。由 theta 爆发刺激诱导的 LTP 和 LTD 出现在以这种方式组织的斑块中，平均而言，LTP 被 LTD 包围。给定颗粒层区域中长期突触可塑性的迹象与兴奋直接相关，与抑制成反比：最活跃的区域倾向于产生LTP，而最不活跃的区域倾向于产生LTD。应用 NMDA 受体阻滞剂 APV 几乎完全阻止了可塑性。这表明突触抑制通过控制膜去极化，有效调节 NMDA 通道的畅通、突触后钙的进入以及苔藓纤维颗粒细胞中继处双向突触可塑性的诱导（Gall 等，2005）。通过这种机制，LTP 和 LTD 可以调节网络计算的几何形状和对比度，预处理要传送到浦肯野细胞和分子层中间神经元的苔藓纤维输入。
The spatial organization of long-term synaptic plasticity [long-term potentiation (LTP) and long-term depression (LTD)] is supposed to play a critical role for distributed signal processing in neuronal networks, but its nature remains undetermined in most central circuits. By using multielectrode array recordings, we have reconstructed activation maps of the granular layer in cerebellar slices. LTP and LTD induced by theta-burst stimulation appeared in patches organized in such a way that, on average, LTP was surrounded by LTD. The sign of long-term synaptic plasticity in a given granular layer region was directly correlated with excitation and inversely correlated with inhibition: the most active areas tended to generate LTP, whereas the least active areas tended to generate LTD. Plasticity was almost entirely prevented by application of the NMDA receptor blocker, APV. This suggests that synaptic inhibition, through a control of membrane depolarization, effectively regulates NMDA channel unblock, postsynaptic calcium entry, and the induction of bidirectional synaptic plasticity at the mossy fiber-granule cell relay (Gall et al., 2005). By this mechanism, LTP and LTD could regulate the geometry and contrast of network computations, preprocessing the mossy fiber input to be conveyed to Purkinje cells and molecular layer interneurons.