Developmental Trajectories of Auditory Cortex Synaptic Structures and Gap-Prepulse Inhibition of Acoustic Startle Between Early Adolescence and Young Adulthood in Mice.
Developmental Trajectories of Auditory Cortex Synaptic Structures and Gap-Prepulse Inhibition of Acoustic Startle Between Early Adolescence and Young Adulthood in Mice.
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DOI：
10.1093/cercor/bhv040
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发表时间：
2016-05
期刊：
影响因子：
3.7
通讯作者：
Caitlin E. Moyer;S. Erickson;K. Fish;E. Thiels;P. Penzes;R. Sweet
中科院分区：
文献类型：
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作者：
Caitlin E. Moyer;S. Erickson;K. Fish;E. Thiels;P. Penzes;R. Sweet
皮质兴奋性和抑制性突触在精神分裂症中被破坏，其症状通常在青春期出现，此时皮质兴奋性突触经历修剪。在听觉皮层，一个与精神分裂症有关的大脑区域，人们对青春期早期和成年早期之间兴奋性和抑制性突触的发展以及这些变化如何影响听觉皮层功能知之甚少。我们使用免疫组织化学和定量荧光显微镜定量树突棘和GAD 65表达抑制扣在早期青春期，晚期青春期和年轻成年小鼠的听觉皮层。在青春期早期和青年期之间，脊柱数量减少，在此期间，听觉皮层依赖的感觉任务中的时间反应增加，无声的间隙-前脉冲抑制声惊吓反射（间隙-PPI）。在青春期后期和青年期之间，终扣内GAD 65蛋白和表达GAD 65的终扣数量减少，相对于脊柱和间隙PPI变化，发病延迟。在缺乏棘蛋白kalirin的小鼠中，青春期和青年期之间的棘数、内扣GAD 65蛋白或gap-PPI没有显著变化。这些结果说明了青春期和青年期之间的听觉皮层棘，抑制钮和听觉皮层功能的发展变化，并提供了深入了解如何中断青少年神经发育可能有助于听觉皮层突触病理和听觉障碍。
Cortical excitatory and inhibitory synapses are disrupted in schizophrenia, the symptoms of which often emerge during adolescence, when cortical excitatory synapses undergo pruning. In auditory cortex, a brain region implicated in schizophrenia, little is known about the development of excitatory and inhibitory synapses between early adolescence and young adulthood, and how these changes impact auditory cortex function. We used immunohistochemistry and quantitative fluorescence microscopy to quantify dendritic spines and GAD65-expressing inhibitory boutons in auditory cortex of early adolescent, late adolescent, and young adult mice. Numbers of spines decreased between early adolescence and young adulthood, during which time responses increased in an auditory cortex-dependent sensory task, silent gap-prepulse inhibition of the acoustic startle reflex (gap-PPI). Within-bouton GAD65 protein and GAD65-expressing bouton numbers decreased between late adolescence and young adulthood, a delay in onset relative to spine and gap-PPI changes. In mice lacking the spine protein kalirin, there were no significant changes in spine number, within-bouton GAD65 protein, or gap-PPI between adolescence and young adulthood. These results illustrate developmental changes in auditory cortex spines, inhibitory boutons, and auditory cortex function between adolescence and young adulthood, and provide insights into how disrupted adolescent neurodevelopment could contribute to auditory cortex synapse pathology and auditory impairments.