SITE-SPECIFIC HYDROGEN SULFIDE-MEDIATED CENTRAL REGULATION OF RESPIRATORY RHYTHM IN MEDULLARY SLICES OF NEONATAL RATS
SITE-SPECIFIC HYDROGEN SULFIDE-MEDIATED CENTRAL REGULATION OF RESPIRATORY RHYTHM IN MEDULLARY SLICES OF NEONATAL RATS
复制标题
硫化氢介导的新生大鼠髓质切片呼吸节律的中枢调节
DOI：
10.1016/j.neuroscience.2012.12.047
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发表时间：
2013-03-13
期刊：
影响因子：
3.3
通讯作者：
Zheng, Y.
中科院分区：
文献类型：
--
作者：
Chen, L.;Zhang, J.;Zheng, Y.
硫化氢（H2S）参与延髓水平呼吸节律的中枢调节。本研究旨在验证我们的假设，即H2S对新生大鼠延髓呼吸节律具有位点特异性调节作用。记录了新生大鼠延髓脑片舌下神经小根的节律性放电。200 μ M NaHS（一种H2S供体）在含有前Botzinger复合物（preBotC）的900 μ m切片中增加了爆发频率（BF），而在含有preBotC和部分或全部面旁呼吸组（pFRG）的1200 μ m、1400 μ m和1800 μ m切片中引起了双相反应：BF最初减少，随后增加。在1400 μ m切片中，在单侧损伤pFRG区域后，不再观察到BF的初始降低。此外，BF增加了单侧微量注射NaHS到preBotC区域，但减少了注射到pFRG区域。这些数据支持我们的假设，即H2S对延髓呼吸节律的调节作用是位点特异性的。兴奋作用由preBotC引起，而抑制作用来自pFRG。(c)2012年IBRO。由爱思唯尔有限公司出版。保留所有权利。
Hydrogen sulfide (H2S) is involved in central regulation of respiratory rhythm at the level of the medulla oblongata. The present study was carried out to test our hypothesis that H2S exerts site-specific regulatory action on respiratory rhythm in the medulla oblongata of neonatal rats. The rhythmic discharge of hypoglossal rootlets in medullary slices of neonatal rats was recorded. 200 mu M NaHS (an H2S donor) increased burst frequency (BF) in 900-mu m slices containing the pre-Botzinger complex (preBotC), whereas it caused diphasic responses in 1200-, 1400- and 1800-mu m slices containing both the preBotC and part or all of the parafacial respiratory group (pFRG): an initial decrease in BF followed by an increase. The initial decrease in BF was no longer observed after unilateral lesion of the pFRG region in the 1400-mu m slices. In addition, BF was increased by a unilateral micro-injection of NaHS into the preBotC region, but was decreased by an injection into the pFRG region. These data support our hypothesis that the regulatory action of H2S on respiratory rhythm in the medulla oblongata is site-specific. The excitatory effect is caused by the preBotC, while the inhibitory effect is from the pFRG. (c) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.