Long-Term Potentiation of Excitatory Synapses on Neocortical Somatostatin-Expressing Interneurons
Long-Term Potentiation of Excitatory Synapses on Neocortical Somatostatin-Expressing Interneurons
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DOI：
10.1152/jn.00641.2009
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发表时间：
2009-12-01
影响因子：
2.5
通讯作者：
Roper, Steven N.
中科院分区：
文献类型：
--
作者：
Chen, Huan-Xin;Jiang, Mali;Roper, Steven N.
陈 H-X，蒋 M，阿卡金 D，罗珀 SN。表达新皮质生长抑素的中间神经元兴奋性突触的长期增强。 J Neurophysiol 102: 3251-3259, 2009。首次发表于 2009 年 9 月 23 日； doi：10.1152/jn.00641.2009。突触可塑性已在新皮质的主要神经元中得到广泛研究，但对 GABA 能中间神经元的研究较少。中间神经元由多种亚型组成，其突触特性因亚型而异。在本研究中，我们使用在这些中间神经元中表达增强的绿色荧光蛋白的转基因小鼠，检查了新皮质中表达生长抑素（SS）的中间神经元的兴奋性突触的长期增强（LTP）。我们发现，在 SS 中间神经元中诱导 LTP 需要强烈的 θ 爆发刺激。 LTP 与配对脉冲促进的减少有关，并且不会被 N-甲基-D-天冬氨酸受体 (NMDAR) 拮抗剂阻断。 LTP 不受用 BAPTA（一种快速 Ca(2+) 螯合剂）螯合突触后 Ca(2) 以及用尼莫地平阻断 L 型电压依赖性 Ca(2+) 通道的影响。使用毛喉素（一种腺苷酸环化酶激活剂）可增加环磷酸腺苷 (cAMP) 浓度，增强突触传递并阻断随后的 LTP 诱导。最后，我们发现 LTP 被蛋白激酶 A (PKA) 抑制剂阻断。我们的结果表明，SS 中间神经元上的兴奋性突触表达突触前形式的 LTP，该形式不依赖于 NMDAR 或突触后 Ca(2+) 升高，而是依赖于 cAMP-PKA 信号通路。
Chen H-X, Jiang M, Akakin D, Roper SN. Long-term potentiation of excitatory synapses on neocortical somatostatin-expressing interneurons. J Neurophysiol 102: 3251-3259, 2009. First published September 23, 2009; doi:10.1152/jn.00641.2009. Synaptic plasticity has been extensively studied in principal neurons of the neocortex, but less work has been done on GABAergic interneurons. Interneurons consist of multiple subtypes and their synaptic properties vary between subtypes. In the present study, we have examined long-term potentiation (LTP) of excitatory synapses on somatostatin (SS)-expressing interneurons in neocortex using transgenic mice that express enhanced green fluorescent protein in these interneurons. We found that a strong theta burst stimulation was required to induce LTP in SS interneurons. LTP was associated with a reduction in paired-pulse facilitation and was not blocked by an N-methyl-D-aspartate receptor (NMDAR) antagonist. LTP was not affected by chelating postsynaptic Ca(2) with BAPTA, a fast Ca(2+) chelator, and blocking L-type voltage-dependent Ca(2+) channels with nimodipine. Application of forskolin, an activator of adenylate cyclase that increases cyclic adenosine monophosphate (cAMP) concentration, enhanced synaptic transmission and occluded subsequent induction of LTP. Finally, we found that LTP was blocked by protein kinase A (PKA) inhibitors. Our results suggest that excitatory synapses on SS interneurons express a presynaptic form of LTP that is not dependent on NMDARs or postsynaptic Ca(2+) rise but is dependent on the cAMP-PKA signaling pathway.