Background. Intermittent hypoxia can induce respiratory neuroplasticity to enhance respiratory motor outputs following hypoxic treatment. This type of respiratory neuroplasticity is primarily mediated by the activation of Gq-protein-coupled 5-HT2 receptors and constrained by Gs-protein-coupled 5-HT7 receptors. Objective. The present study hypothesized that the blockade of 5-HT7 receptors can potentiate the effect of intermittent hypercapnic-hypoxia on respiratory function after cervical spinal cord contusion injury. Methods. The ventilatory behaviors of unanesthetized rats with midcervical spinal cord contusions were measured before, during, and after daily acute intermittent hypercapnic-hypoxia (10 episodes of 5 minutes of hypoxia [10% O2, 4% CO2, 86% N2] with 5 minutes of normoxia intervals for 5 days) at 8 weeks postinjury. On a daily basis, 5 minutes before intermittent hypercapnic-hypoxia, rats received either a 5-HT7 receptor antagonist (SB269970, 4 mg/kg, intraperitoneal) or a vehicle (dimethyl sulfoxide). Results. Treatment with intermittent hypercapnic-hypoxia induced a similar increase in tidal volume between rats that received SB269970 and those that received dimethyl sulfoxide within 60 minutes post-hypoxia on the first day. However, after 2 to 3 days of daily acute intermittent hypercapnic-hypoxia, the baseline tidal volumes of rats treated with SB269970 increased significantly. Conclusions. These results suggest that inhibiting the 5-HT7 receptor can transiently improve daily intermittent hypercapnic-hypoxia–induced tidal volume increase in midcervical spinal contused animals. Therefore, combining pharmacological treatment with rehabilitative intermittent hypercapnic-hypoxia training may be an effective strategy for synergistically enhancing respiratory neuroplasticity to improve respiratory function following chronic cervical spinal cord injury.

中文翻译：

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5-HT7 受体抑制可瞬时改善慢性中颈脊髓挫伤大鼠每日急性间歇性高碳酸血症-缺氧后的呼吸功能

背景。间歇性缺氧可诱导呼吸神经可塑性，以增强缺氧治疗后的呼吸运动输出。这种类型的呼吸神经可塑性主要由 Gq 蛋白偶联 5-HT2 受体的激活介导，并受 Gs 蛋白偶联 5-HT7 受体的限制。客观的。本研究假设阻断 5-HT7 受体可以增强间歇性高碳酸血症缺氧对颈脊髓挫伤后呼吸功能的影响。方法。在每日急性间歇性高碳酸血症缺氧（10 次 5 分钟缺氧 [10% O2、4% CO2、86% N2] 5 分钟）之前、期间和之后测量未麻醉大鼠的中段脊髓挫伤的通气行为。正常氧间隔 5 天）在受伤后 8 周。以一天为周期，在间歇性高碳酸血症缺氧前 5 分钟，大鼠接受 5-HT7 受体拮抗剂（SB269970，4 毫克/千克，腹膜内）或载体（二甲基亚砜）。结果。在缺氧后 60 分钟内，间歇性高碳酸血症缺氧治疗导致接受 SB269970 的大鼠和接受二甲基亚砜的大鼠之间的潮气量增加相似。然而，每天急性间歇性高碳酸血症缺氧 2 到 3 天后，用 SB269970 治疗的大鼠的基线潮气量显着增加。结论。这些结果表明，抑制 5-HT7 受体可以暂时改善中段脊髓挫伤动物的每日间歇性高碳酸血症-缺氧诱导的潮气量增加。所以，