Almado Carlos Eduardo L, Leão Ricardo M, Machado Benedito H
Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, 14049-900, Ribeirão Preto, SP, Brazil.
Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, 14049-900, Ribeirão Preto, SP, Brazil
Exp Physiol. 2014 Jul;99(7):937-50. doi: 10.1113/expphysiol.2013.077800. Epub 2014 Apr 11.
The presympathetic neurons in the rostral ventrolateral medulla (RVLM) are considered to be the source of the sympathetic activity, and there is experimental evidence that these cells present intrinsic autodepolarization. There is also evidence that an important respiratory neuronal population located in the RVLM/Bötzinger complex (BötC) corresponds to augmenting expiratory neurons (aug-E), which send projections to the phrenic nucleus in the spinal cord. However, the pacemaker activity of presympathetic neurons and the intrinsic properties of aug-E neurons had not been evaluated in brainstem slices of juvenile rats (postnatal day 35). Chronic intermittent hypoxia (CIH) is a sympathetic-mediated hypertension model, which seems to produce an associated increase in the activity of aug-E neurons. In this study, we evaluated the effects of CIH on the intrinsic properties of RVLM/BötC presympathetic and phrenic nucleus-projecting neurons (aug-E) in brainstem slices of juvenile rats (postnatal day 35). We observed that all presympathetic neurons presented spontaneous action potential firing (n = 18), which was not abolished by ionotropic receptor antagonism. In addition, exposure to 10 days of CIH produced no changes in their intrinsic passive properties, firing pattern or excitability. Most aug-E neurons presented spontaneous firing in control conditions (13 of 15 neurons), and this characteristic was preserved after blocking fast synaptic transmission (12 of 15 neurons), clearly demonstrating their intrinsic pacemaker activity. Chronic intermittent hypoxia also produced no changes in intrinsic passive properties, frequency and pattern of discharge or excitability of the aug-E neurons. The present study shows that: (i) it is possible to record the electrophysiological properties of RVLM/BötC presympathetic and aug-E neurons in brainstem slices from juvenile rats; (ii) these neurons present characteristics of intrinsic pacemakers; and (iii) their intrinsic properties were not altered by chronic intermittent hypoxia.
延髓头端腹外侧区（RVLM）中的交感神经节前神经元被认为是交感神经活动的来源，并且有实验证据表明这些细胞存在内在的自动去极化现象。也有证据表明，位于RVLM/包钦格复合体（BötC）中的一个重要呼吸神经元群对应于增强呼气神经元（aug-E），这些神经元向脊髓中的膈神经核发送投射。然而，交感神经节前神经元的起搏活动和aug-E神经元的内在特性在幼年大鼠（出生后第35天）的脑干切片中尚未得到评估。慢性间歇性缺氧（CIH）是一种交感神经介导的高血压模型，似乎会导致aug-E神经元的活动相应增加。在本研究中，我们评估了CIH对幼年大鼠（出生后第35天）脑干切片中RVLM/BötC交感神经节前和膈神经核投射神经元（aug-E）内在特性的影响。我们观察到，所有交感神经节前神经元均呈现出自发动作电位发放（n = 18），离子型受体拮抗作用并未消除这种发放。此外，暴露于10天的CIH对其内在被动特性、发放模式或兴奋性没有产生影响。大多数aug-E神经元在对照条件下呈现出自发发放（15个神经元中的13个），在阻断快速突触传递后这一特性仍然保留（15个神经元中的12个），清楚地证明了它们的内在起搏活动。慢性间歇性缺氧对aug-E神经元的内在被动特性、放电频率和模式或兴奋性也没有产生影响。本研究表明：（i）有可能在幼年大鼠的脑干切片中记录RVLM/BötC交感神经节前和aug-E神经元的电生理特性；（ii）这些神经元呈现出内在起搏细胞的特征；（iii）它们的内在特性不会因慢性间歇性缺氧而改变。
