Purkinje cell degeneration elevates eupneic and hypercapnic ventilation in rats.
Purkinje cell degeneration elevates eupneic and hypercapnic ventilation in rats.
复制标题
浦肯野细胞变性可提高大鼠的正常通气和高碳酸血症通气。
DOI：
10.1080/14734220310023332
复制
发表时间：
2004
期刊：
影响因子：
--
通讯作者：
Frazier,DonaldT
中科院分区：
文献类型：
--
作者：
Xu,Fadi;Zhou,Tongrong;Frazier,DonaldT
Previous studies have demonstrated that among cerebellar nuclei, the fastigial nucleus (FN) plays a major role in facilitation of respiration, especially during hypercapnia. Since the FN primarily receives inhibitory afferents from Purkinje cells (PCs), we hypothesized that degeneration of PCs would increase both eupneic and hypercapnic ventilation. Experiments were carried out on 20 animals (n=10 for both normal and PC-degenerated) that were divided into three groups based on the different preparations used, i.e., four pairs for the awake, three pairs for the anesthetized, and three other pairs initially for the awake and subsequently for the anesthetized. The awake normal and PCD rats were separately placed in an unrestrained whole-body plethysmograph and ventilatory parameters measured before (room air) and during hypercapnia (5% CO2+ 21% O2+ 74% N2) for 30 min. The anesthetized animals were exposed to the same level of hypercapnia applied for ∼5 min. The results showed that both eupneic breathing and hypercapnia-induced ventilatory augmentation were significantly greater in the awake PCD rat than those observed in the normal one, primarily due to a remarkable elevation in VTwith little changes inf. The same results were also observed in anesthetized preparations. A Fos protein immunocytochemical approach was employed to determine the effect of degeneration on PCs and FN neuronal activity. Fos expression of PCs was very intensive in normal rats, but absent or diminished in PCD rats. In sharp contrast, FN Fos expression was obscure in normal rats, but very apparent in PCD rats. These data suggest that PCs play an inhibitory role in modulation of eupneic and hypercapnic ventilation via inhibiting FN neuronal activity.
