Physical (in)activity-dependent structural plasticity in bulbospinal catecholaminergic neurons of rat rostral ventrolateral medulla.

Physical (in)activity-dependent structural plasticity in bulbospinal catecholaminergic neurons of rat rostral ventrolateral medulla.
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DOI:
10.1002/cne.23464
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发表时间:
2014-02-15
期刊:
The Journal of comparative neurology
影响因子:
--
通讯作者:
Mueller PJ
Mueller PJ
中科院分区:
其他
文献类型:
--
作者:
Mischel NA;Llewellyn-Smith IJ;Mueller PJ

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交感神经系统的活动增加被认为在心血管疾病的发展和进展中起作用。最近的研究表明,与活动相比,身体不活动会改变与心血管调节相关的大脑区域的神经元结构。我们的生理学研究表明,在延髓头端腹外侧(RVLM)的神经元更敏感的兴奋久坐与体力活动的动物。我们推测,RVLM中增强的功能反应可能部分是由于控制交感神经活动的RVLM神经元结构的变化。我们采用逆行追踪和酪氨酸羟化酶(TH)的免疫组织化学方法,以确定长期自愿轮跑运动后久坐和活动大鼠的球脊髓儿茶酚胺(C1)神经元。然后,我们在不同的吻尾水平数字重建他们的细胞体和树突。运动组大鼠脊髓投射TH神经元的树突分支明显多于运动组大鼠(p<0.05)。在久坐不动的大鼠,树突状分支是更大的喙部与更多的尾部球脊髓C1神经元,而在体力活动的大鼠,树突状分支是一致的整个RVLM。相比之下,活跃和不活跃的动物之间的细胞体大小和初级树突的数量没有差异。我们认为,这些结构的变化提供了一个解剖学基础的功能差异,在我们的体内研究中观察到的。这些与失活相关的结构和功能变化增强了RVLM神经元对兴奋性刺激的整体敏感性,并可能导致久坐个体患心血管疾病的风险增加。与活动相比,身体不活动与延髓头端腹外侧(RVLM)神经元控制血压的功能变化有关。在这里,作者表明,假定的心血管RVLM神经元有更复杂的树突在不活跃与活跃的大鼠。这种解剖学差异可能是以前报道的功能差异的基础。
Increased activity of the sympathetic nervous system is thought to play a role in the development and progression of cardiovascular disease. Recent work has shown that physical inactivity versus activity alters neuronal structure in brain regions associated with cardiovascular regulation. Our physiological studies suggest that neurons in the rostral ventrolateral medulla (RVLM) are more responsive to excitation in sedentary versus physically active animals. We hypothesized that enhanced functional responses in the RVLM may be due, in part, to changes in the structure of RVLM neurons that control sympathetic activity. We used retrograde tracing and immunohistochemistry for tyrosine hydroxylase (TH) to identify bulbospinal catecholaminergic (C1) neurons in sedentary and active rats after chronic voluntary wheel-running exercise. We then digitally reconstructed their cell bodies and dendrites at different rostrocaudal levels. The dendritic arbors of spinally-projecting TH neurons from sedentary rats were more branched than those of physically active rats (p<0.05). In sedentary rats, dendritic branching was greater in more rostral versus more caudal bulbospinal C1 neurons whereas, in physically active rats, dendritic branching was consistent throughout the RVLM. In contrast, cell body size and the number of primary dendrites did not differ between active and inactive animals. We suggest that these structural changes provide an anatomical underpinning for the functional differences observed in our in vivo studies. These inactivity-related structural and functional changes enhance the overall sensitivity of RVLM neurons to excitatory stimuli and may contribute to an increased risk of cardiovascular disease in sedentary individuals. Physical inactivity versus activity is associated with functional changes in control of blood pressure by neurons in the rostral ventrolateral medulla (RVLM). Here, the authors show that putative cardiovascular RVLM neurons have more complex dendrites in inactive versus active rats. This anatomical difference may underpin the functional differences previously reported.
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