Brain Science Institute RIKEN, Wako, 351-0198 Japan, PRESTO, Japan Science and Technology Agency, Tokyo, 102-0075 Japan.
J Neurosci. 2013 May 1;33(18):7787-98. doi: 10.1523/JNEUROSCI.5350-12.2013.
Most neurons in layer VI of the visual cortex project to the dorsal lateral geniculate nucleus (dLGN). These corticogeniculate projection neurons (CG cells) receive top-down synaptic inputs from upper layers (ULs) and bottom-up inputs from the underlying white matter (WM). Use-dependent plasticity of these synapses in layer VI of the cortex has received less attention than in other layers. In the present study, we used a retrograde tracer injected into dLGN to identify CG cells, and, by analyzing EPSPs evoked by electrical stimulation of the UL or WM site, examined whether these synapses show long-term synaptic plasticity. Theta-burst stimulation induced long-term potentiation (LTP) of activated synapses (hom-LTP) and long-term depression (LTD) of nonactivated synapses (het-LTD) in either pathway. The paired-pulse stimulation protocol and the analysis of coefficient variation of EPSPs suggested postsynaptic induction of these changes except UL-induced het-LTD, which may be presynaptic in origin. Intracellular injection of a Ca(2+)-chelator suggested an involvement of postsynaptic Ca(2+) rise in all types of long-term plasticity. Pharmacological analysis indicated that NMDA receptors and type-5 metabotropic glutamate receptors are involved in WM-induced and UL-induced plasticity, respectively. Analysis with inhibitors and/or in transgenic mice suggested an involvement of cannabinoid type 1 receptors and calcineurin in UL-induced and WM-induced het-LTD, respectively. These results suggest that hom-LTP and het-LTD may play a role in switching the top-down or bottom-up regulation of CG cell function and/or in maintaining stability of synaptic transmission efficacy through different molecular mechanisms.
大多数视觉皮层 VI 层的神经元投射到背外侧膝状体核 (dLGN)。这些皮质-膝状体投射神经元 (CG 细胞) 从上层 (ULs) 接收自上而下的突触输入,从下面的白质 (WM) 接收自下而上的输入。与其他层相比,皮层 VI 层这些突触的依赖使用的可塑性受到的关注较少。在本研究中,我们使用逆行示踪剂注射到 dLGN 来识别 CG 细胞,并通过分析 UL 或 WM 部位电刺激引起的 EPSP,检查这些突触是否表现出长期突触可塑性。θ爆发刺激诱导激活突触的长时程增强 (LTP)(同源 LTP)和非激活突触的长时程抑制 (LTD)(异源 LTD)在两种途径中均有发生。成对脉冲刺激方案和 EPSP 变异系数分析表明,这些变化是突触后诱导的,除了 UL 诱导的异源 LTD 可能是突触前起源的。细胞内注射 Ca(2+) 螯合剂表明,所有类型的长期可塑性都涉及突触后 Ca(2+) 升高。药理学分析表明,NMDA 受体和 5 型代谢型谷氨酸受体分别参与 WM 诱导和 UL 诱导的可塑性。抑制剂和/或转基因小鼠的分析表明,大麻素 1 型受体和钙调神经磷酸酶分别参与 UL 诱导和 WM 诱导的异源 LTD。这些结果表明,同源 LTP 和异源 LTD 可能通过不同的分子机制在 CG 细胞功能的自上而下或自下而上调节的转换中发挥作用,或者在维持突触传递效能的稳定性中发挥作用。