Deprivation-Induced Strengthening of Presynaptic and Postsynaptic Inhibitory Transmission in Layer 4 of Visual Cortex during the Critical Period
Deprivation-Induced Strengthening of Presynaptic and Postsynaptic Inhibitory Transmission in Layer 4 of Visual Cortex during the Critical Period
复制标题
DOI：
10.1523/jneurosci.4600-13.2014
复制
发表时间：
2014-02-12
影响因子：
5.3
通讯作者：
Turrigiano, Gina G.
中科院分区：
文献类型：
--
作者：
Nahmani, Marc;Turrigiano, Gina G.
抑制从快速尖峰（FS）interneurons起着至关重要的作用，在塑造皮质反应特性和门控活动依赖性可塑性的发展时期，但FS抑制可塑性的表达机制仍然在很大程度上未被探索。在视觉皮层（V1）的第4层中，单眼剥夺（MD）诱导FS至星星锥体神经元（FS -> SP）突触的抑制或增强，这取决于发病年龄（Maffei et al.，2004年、2006年）。塑性的符号（-到+）的这种反转发生在典型临界期（CP）的尖点。为了研究这种抑制可塑性信号转换背后的表达位点，小鼠在前CP [睁眼至出生后第17天（p）]或CP（p22-p25）期间经历MD，并且使用共聚焦和免疫电子显微镜以及FS细胞的光遗传学激活来探测FS -> SP突触处的量子幅度，评估第4层内FS -> SP突触强度。在p17或p25之前的BriefMD没有改变FS -> SP接触的密度。然而，在超微结构水平上，与非剥夺对照半球的突触相比，在CP期间剥夺半球的FS -> SP突触具有更大的突触和更高的停靠囊泡密度，而在CP前或GAD（65）基因敲除小鼠中则没有。此外，当CP期间MD启动时，FS -> SP诱发剥夺半球的微型IPSC增加，并伴有FS -> SP突触的突触后GABA（A）受体密度增加。这些FS -> SP突触强度的协调变化定义了视皮层CP可塑性过程中调节兴奋性输出的表达途径。
Inhibition from fast-spiking (FS) interneurons plays a crucial role in shaping cortical response properties and gating developmental periods of activity-dependent plasticity, yet the expression mechanisms underlying FS inhibitory plasticity remain largely unexplored. In layer 4 of visual cortex (V1), monocular deprivation (MD) induces either depression or potentiation of FS to star pyramidal neuron (FS -> SP) synapses, depending on the age of onset (Maffei et al., 2004, 2006). This reversal in the sign (- to +) of plasticity occurs on the cusp of the canonical critical period (CP). To investigate the expression locus behind this switch in sign of inhibitory plasticity, mice underwentMDduring the pre-CP [eye-opening to postnatal day (p) 17] or CP (p22-p25), and FS -> SP synaptic strength within layer 4 was assessed using confocal and immunoelectron microscopy, as well as optogenetic activation of FS cells to probe quantal amplitude at FS -> SP synapses. BriefMDbefore p17 or p25 did not alter the density of FS -> SP contacts. However, at the ultrastructural level, FS -> SP synapses in deprived hemispheres during the CP, but not the pre-CP or in GAD(65) knock-out mice, had larger synapses and increased docked vesicle density compared with synapses from the nondeprived control hemispheres. Moreover, FS -> SP evoked miniature IPSCs increased in deprived hemispheres when MD was initiated during the CP, accompanied by an increase in the density of postsynaptic GABA(A) receptors at FS -> SP synapses. These coordinated changes in FS -> SP synaptic strength define an expression pathway modulating excitatory output during CP plasticity in visual cortex.