PDF(Pubmed)
Abstract：
Plasticity is a hallmark of the respiratory neural control system. Phrenic long-term facilitation (pLTF) is one form of respiratory plasticity characterized by persistent increases in phrenic nerve activity following acute intermittent hypoxia (AIH). Although there is evidence that key steps in the cellular pathway giving rise to pLTF are localized within phrenic motor neurons (PMNs), the impact of AIH on the strength of breathing-related synaptic inputs to PMNs remains unclear. Furthermore, the functional impact of AIH is enhanced by repeated/daily exposure to AIH (dAIH). Here, we explored the effects of AIH versus 2 wk of dAIH preconditioning on spontaneous and evoked phrenic responses in anesthetized, paralyzed, and mechanically ventilated rats. Evoked phrenic potentials were elicited by respiratory cycle-triggered lateral funiculus stimulation at the C2 spinal level delivered before and 60 min post-AIH (or the equivalent in time controls). Charge-balanced biphasic pulses (100 μs/phase) of progressively increasing intensity (100-700 μA) were delivered during the inspiratory and expiratory phases of the respiratory cycle. Although robust pLTF (∼60% from baseline) was observed after a single exposure to moderate AIH (3 × 5 min; 5-min intervals), there was no effect on evoked phrenic responses, contrary to our initial hypothesis. However, in rats preconditioned with dAIH, baseline phrenic nerve activity and evoked responses were increased, suggesting that repeated exposure to AIH enhances functional synaptic strength when assessed using this technique. The impact of daily AIH preconditioning on synaptic inputs to PMNs raises interesting questions that require further exploration.NEW & NOTEWORTHY Two weeks of daily acute intermittent hypoxia (dAIH) preconditioning enhanced stimulus-evoked phrenic responses to lateral funiculus stimulation (targeting respiratory bulbospinal projection to phrenic motor neurons). Furthermore, dAIH preconditioning enhanced baseline phrenic motor output responses to maximal chemoreflex activation in intact rats.
摘要：
可塑性是呼吸神经控制系统的标志。膈长期促进（pLTF）是呼吸可塑性的一种形式，其特征是急性间歇性缺氧（AIH）后膈神经活动持续增加。尽管有证据表明，引起pLTF的细胞途径中的关键步骤位于膈运动神经元（PMN）内，AIH对PMN呼吸相关突触输入强度的影响尚不清楚.此外，AIH的功能影响通过重复/每日暴露于AIH(dAIH)而增强。这里,我们探讨了AIH与2周dAIH预处理对麻醉中自发和诱发膈反应的影响，瘫痪,和机械通气的大鼠。在AIH之前和之后60分钟（或等效的时间控制）传递的C2脊髓水平上，通过呼吸周期触发的侧索刺激引起膈电位。在呼吸周期的吸气和呼气阶段，传递了强度逐渐增加（100-700μA）的电荷平衡的双相脉冲（100μs/相）。尽管在单次暴露于中度AIH（3×5分钟；5分钟间隔）后观察到稳健的pLTF（~基线为60%），对诱发的膈反应没有影响，与我们最初的假设相反。然而,在用dAIH预处理的大鼠中，基线膈神经活动和诱发反应增加，提示当使用该技术评估时,反复暴露于AIH可增强功能性突触强度.每日AIH预处理对PMN突触输入的影响提出了需要进一步探索的有趣问题。NEW&NOTEWORTHY两周每日急性间歇性缺氧(dAIH)预处理增强刺激诱发的膈肌对外侧肌刺激的反应(针对膈运动神经元的呼吸延髓投射)。此外，dAIH预处理增强了完整大鼠对最大化学反射激活的基线膈运动输出反应。
