Glutamatergic Antagonism in the NTS Decreases Post-Inspiratory Drive and Changes Phrenic and Sympathetic Coupling During Chemoreflex Activation
Glutamatergic Antagonism in the NTS Decreases Post-Inspiratory Drive and Changes Phrenic and Sympathetic Coupling During Chemoreflex Activation
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DOI：
10.1152/jn.00802.2009
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发表时间：
2010-04-01
影响因子：
2.5
通讯作者：
Machado, Benedito H.
中科院分区：
文献类型：
--
作者：
Costa-Silva, Joao H.;Zoccal, Daniel B.;Machado, Benedito H.
Costa-Silva JH，Zoccal DB，马查多BH. NTS中的谷氨酸能拮抗作用降低吸气后驱动，并在化学反射激活期间改变膈神经和交感神经耦合。J Neurophysiol 103：2095-2106，2010.首次发表于2010年2月17日; doi：10.1152/jn.00802.2009。为了更好地理解在孤束核（NTS）水平的自主神经和呼吸反应的外周化学感受器激活的处理，在此，我们评估了中间（iNTS）和尾侧NTS（cNTS）中的多巴胺能神经传递的作用，基线呼吸参数和化学反射诱发的反应，使用在原位工作的心-脑干准备（WHBP）。在双侧iNTS、cNTS或同时注射犬尿烯酸（Kyn，5 nmol/20 nl）前后记录膈神经（PND）、颈迷走神经（cVNA）和胸交感神经（tSNA）的活动。在WHBP中，基线交感神经放电与膈神经爆发（吸气）显著相关。然而，大多数化学反射激活引起的交感兴奋发生在呼气。iNTS或cNTS内微量注射Kyn可减少cVNA的吸气后成分，增加PND的持续时间和频率。Kyn到iNTS产生外周化学反射激活的交感神经兴奋和呼吸急促反应没有变化，而到cNTS，观察到交感神经兴奋减少，但呼吸急促没有减少。膈神经和交感神经耦合的模式在化学反射激活吸气相关，而不是呼气相关的交感兴奋。Kyn同时进入iNTS和cNTS产生更大的cVNA的吸气后成分的减少和PND的频率和持续时间的增加，并取消呼吸和自主神经反应的化学反射激活。数据显示，iNTS和cNTS中的交感神经传递对基线呼吸节律起着滋补作用，有助于吸气后活动，并且对于化学反射激活期间观察到的呼气相关交感兴奋至关重要。
Costa-Silva JH, Zoccal DB, Machado BH. Glutamatergic antagonism in the NTS decreases post-inspiratory drive and changes phrenic and sympathetic coupling during chemoreflex activation. J Neurophysiol 103: 2095-2106, 2010. First published February 17, 2010; doi: 10.1152/jn.00802.2009. For a better understanding of the processing at the nucleus tractus solitarius (NTS) level of the autonomic and respiratory responses to peripheral chemoreceptor activation, herein we evaluated the role of glutamatergic neurotransmission in the intermediate (iNTS) and caudal NTS (cNTS) on baseline respiratory parameters and on chemoreflex-evoked responses using the in situ working heart-brain stem preparation (WHBP). The activities of phrenic (PND), cervical vagus (cVNA), and thoracic sympathetic (tSNA) nerves were recorded before and after bilateral microinjections of kynurenic acid (Kyn, 5 nmol/20 nl) into iNTS, cNTS, or both simultaneously. In WHBP, baseline sympathetic discharge markedly correlated with phrenic bursts (inspiration). However, most of sympathoexcitation elicited by chemoreflex activation occurred during expiration. Kyn microinjected into iNTS or into cNTS decreased the postinspiratory component of cVNA and increased the duration and frequency of PND. Kyn into iNTS produced no changes in sympathoexcitatory and tachypneic responses to peripheral chemoreflex activation, whereas into cNTS, a reduction of the sympathoexcitation, but not of the tachypnea, was observed. The pattern of phrenic and sympathetic coupling during the chemoreflex activation was an inspiratory-related rather than an expiratory-related sympathoexcitation. Kyn simultaneously into iNTS and cNTS produced a greater decrease in postinspiratory component of cVNA and increase in frequency and duration of PND and abolished the respiratory and autonomic responses to chemoreflex activation. The data show that glutamatergic neurotransmission in the iNTS and cNTS plays a tonic role on the baseline respiratory rhythm, contributes to the postinspiratory activity, and is essential to expiratory-related sympathoexcitation observed during chemoreflex activation.