Somatostatin neuron contributions to cortical slow wave dysfunction in adult mice exposed to developmental ethanol.
Somatostatin neuron contributions to cortical slow wave dysfunction in adult mice exposed to developmental ethanol.
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DOI：
10.3389/fnins.2023.1127711
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发表时间：
2023
影响因子：
4.3
通讯作者：
Saito, Mariko
中科院分区：
文献类型：
--
作者：
Wilson, Donald A.;Fleming, G.;Williams, C. R. O.;Teixeira, C. M.;Smiley, J. F.;Saito, Mariko
关键词：
睡眠和清醒之间的转换以及睡眠依赖的皮层振荡严重依赖gaba能神经元。重要的是，gaba能神经元对发育中的乙醇暴露特别敏感，这表明睡眠回路对早期乙醇具有潜在的独特脆弱性。事实上，发育性酒精暴露会对睡眠造成长期损害，包括增加睡眠碎片和减少δ波振幅。在这里，我们评估了光基因操作在P7暴露于生理盐水或乙醇的成年小鼠新皮质中生长抑素（SST） gaba能神经元调节皮质慢波生理的效果。将SST-cre × Ai32小鼠在P7上暴露于乙醇或生理盐水中，SST-cre × Ai32小鼠选择性表达SST神经元通道视紫红质。该品系表现出与C57BL/6By小鼠相似的发育性乙醇诱导的SST皮质神经元丢失和睡眠障碍。作为成年人，研究人员将光纤植入前额叶皮层（PFC），并在新皮层植入遥测电极，以监测慢波活动和睡眠-觉醒状态。光刺激PFC SST神经元在生理盐水处理小鼠中诱发慢波电位和长潜伏期单单位兴奋，而在乙醇处理小鼠中则没有。PFC SST神经元自发慢波激活的闭环光遗传刺激增强了皮质δ振荡，这种操作在生理盐水小鼠中比P7乙醇小鼠更有效。综上所述，这些结果表明SST皮质神经元可能参与了发育酒精后的慢波损伤。
Transitions between sleep and waking and sleep-dependent cortical oscillations are heavily dependent on GABAergic neurons. Importantly, GABAergic neurons are especially sensitive to developmental ethanol exposure, suggesting a potential unique vulnerability of sleep circuits to early ethanol. In fact, developmental ethanol exposure can produce long-lasting impairments in sleep, including increased sleep fragmentation and decreased delta wave amplitude. Here, we assessed the efficacy of optogenetic manipulations of somatostatin (SST) GABAergic neurons in the neocortex of adult mice exposed to saline or ethanol on P7, to modulate cortical slow-wave physiology. SST-cre × Ai32 mice, which selectively express channel rhodopsin in SST neurons, were exposed to ethanol or saline on P7. This line expressed similar developmental ethanol induced loss of SST cortical neurons and sleep impairments as C57BL/6By mice. As adults, optical fibers were implanted targeting the prefrontal cortex (PFC) and telemetry electrodes were implanted in the neocortex to monitor slow-wave activity and sleep-wake states. Optical stimulation of PFC SST neurons evoked slow-wave potentials and long-latency single-unit excitation in saline treated mice but not in ethanol mice. Closed-loop optogenetic stimulation of PFC SST neuron activation on spontaneous slow-waves enhanced cortical delta oscillations, and this manipulation was more effective in saline mice than P7 ethanol mice. Together, these results suggest that SST cortical neurons may contribute to slow-wave impairment after developmental ethanol.
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