Miller Justin Robert, Neumueller Suzanne, Muere Clarissa, Olesiak Samantha, Pan Lawrence, Bukowy John D, Daghistany Asem O, Hodges Matthew R, Forster Hubert V
Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin;
Department of Physical Therapy, Marquette University, Milwaukee, Wisconsin;
J Appl Physiol (1985). 2014 Jun 15;116(12):1531-42. doi: 10.1152/japplphysiol.00216.2014. Epub 2014 May 1.
The mechanisms which contribute to the time-dependent recovery of resting ventilation and the ventilatory CO2 chemoreflex after carotid body denervation (CBD) are poorly understood. Herein we tested the hypothesis that there are time-dependent changes in the expression of specific AMPA, NMDA, and/or neurokinin-1 (NK1R) receptors within respiratory-related brain stem nuclei acutely or chronically after CBD in adult goats. Brain stem tissues were collected acutely (5 days) or chronically (30 days) after sham or bilateral CBD, immunostained with antibodies targeting AMPA (GluA1 or GluA2), NMDA (GluN1), or NK-1 receptors, and optical density (OD) compared. Physiological measurement confirmed categorization of each group and showed ventilatory effects consistent with bilateral CBD (Miller et al. J Appl Physiol 115: 1088-1098, 2013). Acutely after CBD, GluA1 OD was unchanged or slightly increased, but GluA2 and GluN1 OD were reduced 15-30% within the nucleus tractus solitarius (NTS) and in other medullary respiratory nuclei. Chronically after CBD, GluA1 was reduced (P < 0.05) within the caudal NTS and in other nuclei, but there was significant recovery of GluA2 and GluN1 OD. NK1 OD was not significantly different from control after CBD. We conclude that the initial decrease in GluA2 and GluN1 after CBD likely contributes to hypoventilation and the reduced CO2 chemoreflex. The partial recovery of ventilation and the CO2 chemoreflex after CBD parallel a time-dependent return of these receptors to near control levels but likely depend upon additional initiating and maintenance factors for neuroplasticity.
目前对颈动脉体去神经支配(CBD)后静息通气和通气二氧化碳化学反射随时间恢复的机制了解甚少。在此,我们测试了一个假设,即在成年山羊急性或慢性CBD后,呼吸相关脑干核内特定的α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)、N-甲基-D-天冬氨酸(NMDA)和/或神经激肽-1(NK1R)受体的表达存在时间依赖性变化。在假手术或双侧CBD后急性(5天)或慢性(30天)收集脑干组织,用靶向AMPA(GluA1或GluA2)、NMDA(GluN1)或NK-1受体的抗体进行免疫染色,并比较光密度(OD)。生理测量证实了每组的分类,并显示出与双侧CBD一致的通气效应(Miller等人,《应用生理学杂志》115: 1088 - 1098,2013)。CBD后急性时,孤束核(NTS)和其他延髓呼吸核内的GluA1 OD未改变或略有增加,但GluA2和GluN1 OD降低了15 - 30%。CBD后慢性时,尾侧NTS和其他核内的GluA1降低(P < 0.05),但GluA2和GluN1 OD有显著恢复。CBD后NK1 OD与对照组无显著差异。我们得出结论,CBD后GluA2和GluN1的最初降低可能导致通气不足和二氧化碳化学反射减弱。CBD后通气和二氧化碳化学反射的部分恢复与这些受体随时间回到接近对照水平平行,但可能依赖于神经可塑性的其他启动和维持因素。