老年大鼠心脏神经节中迷走神经传出轴突和终末的退变。
Degeneration of vagal efferent axons and terminals in cardiac ganglia of aged rats.
作者信息
Ai Jing, Gozal David, Li Lihua, Wead William B, Chapleau Mark W, Wurster Robert, Yang Baofeng, Li Hulun, Liu Rugao, Cheng Zixi
机构信息
Biomolecular Science Center, Burnett College of Biomedical Sciences, University of Central Florida, Orlando, Florida 32816, USA.
出版信息
J Comp Neurol. 2007 Sep 1;504(1):74-88. doi: 10.1002/cne.21431.
Baroreflex control of the heart rate is significantly reduced during aging. However, neural mechanisms that underlie such a functional reduction are not fully understood. We injected the tracer DiI into the left nucleus ambiguus (NA), then used confocal microscopy and a Neurolucida Digitization System to examine qualitatively and quantitatively vagal efferent projections to cardiac ganglia of young adult (5-6 months) and aged (24-25 months) rats (Sprague Dawley). Fluoro-Gold was injected intraperitoneally to counterstain cardiac ganglionic principal neurons (PNs). In aged, as in young rats, NA axons projected to all cardiac ganglia and formed numerous basket endings around PNs in the hearts. However, significant structural changes were found in aged rats compared with young rats. Vagal efferent axons contained abnormally swollen axonal segments and exhibited reduced or even absent synaptic-like terminals around PNs, such that the numbers of vagal fibers and basket endings around PNs were substantially reduced (P < 0.01). Furthermore, synaptic-like varicose contacts of vagal cardiac axons with PNs were significantly reduced by approximately 50% (P < 0.01). These findings suggest that vagal efferents continue to maintain homeostatic control over the heart during aging. However, the marked morphological reorganization of vagal efferent axons and terminals in cardiac ganglia may represent the structural substrate for reduced vagal control of the heart rate and attenuated baroreflex function during aging.
在衰老过程中,压力反射对心率的控制显著降低。然而,导致这种功能降低的神经机制尚未完全明确。我们将示踪剂DiI注入左侧疑核(NA),然后使用共聚焦显微镜和Neurolucida数字化系统,对年轻成年(5 - 6个月)和老年(24 - 25个月)大鼠(Sprague Dawley)心脏神经节的迷走神经传出投射进行定性和定量研究。腹腔注射荧光金对心脏神经节的主要神经元(PNs)进行复染。与年轻大鼠一样,老年大鼠的NA轴突投射到所有心脏神经节,并在心脏的PNs周围形成大量篮状终末。然而,与年轻大鼠相比,老年大鼠出现了显著的结构变化。迷走神经传出轴突包含异常肿胀的轴突节段,并且在PNs周围表现出减少甚至缺失的突触样终末,使得PNs周围的迷走神经纤维数量和篮状终末显著减少(P < 0.01)。此外,迷走心脏轴突与PNs的突触样曲张接触显著减少了约50%(P < 0.01)。这些发现表明,在衰老过程中迷走神经传出纤维继续对心脏维持稳态控制。然而,心脏神经节中迷走神经传出轴突和终末的明显形态重组可能是衰老过程中迷走神经对心率控制减弱和压力反射功能衰减的结构基础。