Impaired long-term memory, a complication of traumatic stress including hemorrhage shock and resuscitation (HSR), has been reported to be associated with multiple neurodegenerations. The ventral tegmental area (VTA) participates in both learned appetitive and aversive behaviors. In addition to being prospective targets for the therapy of addiction, depression, and other stress-related diseases, VTA glutamatergic neurons are becoming more widely acknowledged as powerful regulators of reward and aversion. This study revealed that HSR exposure induces memory impairments and decreases the activation in glutamatergic neurons, and decreased β power in the VTA. We also found that optogenetic activation of glutamatergic neurons in the VTA mitigated HSR-induced memory impairments, and restored β power. Moreover, hydrogen sulfide (HS), a gasotransmitter with pleiotropic roles, has neuroprotective functions at physiological concentrations. In vivo, HS administration improved HSR-induced memory deficits, elevated c-fos-positive vesicular glutamate transporters (Vglut2) neurons, increased β power, and restored the balance of γ-aminobutyric acid (GABA) and glutamate in the VTA. This work suggests that glutamatergic neuron stimulation via optogenetic assay and exogenous HS may be useful therapeutic approaches for improving memory deficits following HSR.

中文翻译：

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硫化氢通过恢复失血性休克和复苏小鼠模型中的谷氨酸能神经元来减轻记忆障碍

据报道，长期记忆受损是包括失血性休克和复苏 (HSR) 在内的创伤应激的并发症，与多种神经退行性疾病有关。腹侧被盖区（VTA）参与习得的食欲和厌恶行为。除了成为成瘾、抑郁症和其他压力相关疾病治疗的潜在靶点外，VTA 谷氨酸能神经元也被越来越广泛地认为是奖赏和厌恶的强大调节器。这项研究表明，HSR 暴露会导致记忆障碍，降低谷氨酸能神经元的激活，并降低 VTA 的 β 功率。我们还发现 VTA 中谷氨酸能神经元的光遗传学激活减轻了 HSR 引起的记忆障碍，并恢复了 β 功率。此外，硫化氢（HS）是一种具有多效作用的气体递质，在生理浓度下具有神经保护功能。在体内，HS给药改善了HSR诱导的记忆缺陷，升高了c-fos阳性囊泡谷氨酸转运蛋白（Vglut2）神经元，增加了β功率，并恢复了VTA中γ-氨基丁酸（GABA）和谷氨酸的平衡。这项工作表明，通过光遗传学测定和外源 HS 刺激谷氨酸能神经元可能是改善 HSR 后记忆缺陷的有效治疗方法。