Posterior hypothalamic modulation of the respiratory response to CO2 in cats.
Posterior hypothalamic modulation of the respiratory response to CO2 in cats.
复制标题
下丘脑后部调节猫对二氧化碳的呼吸反应。
DOI：
10.1007/bf00370445
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Waldrop,TG
中科院分区：
文献类型：
--
作者：
Waldrop,TG
几项研究已经提供了证据，表明桥上结构参与调节对二氧化碳增加的呼吸反应。然而，导致这种效应的实际神经解剖部位(S)尚未确定。因此，本研究的目的是确定下丘脑后部是否是参与调节高碳酸血症呼吸反应的一个吻部部位。在麻醉猫下丘脑后部微量注射γ-氨基丁酸拮抗剂前后，记录其对潮汐末期PCO2递进性阶跃增加的膈神经反应。微量注射拮抗剂可降低呼吸暂停阈值，降低终末二氧化碳分压。此外，微量注射GABA拮抗剂后，膈神经对呼吸暂停阈值以上二氧化碳变化的反应增强。这种增强是由于呼吸频率反应较大，潮汐膈反应略有增加所致。将GABA激动剂微量注射到下丘脑的同一部位，可逆转GABA拮抗剂的作用。没有预先注射拮抗剂的情况下微量注射GABA激动剂没有任何效果。这些结果表明，麻醉猫对呼吸暂停阈值以上二氧化碳分压升高的呼吸反应是由下丘脑后部神经元调节的。这种下丘脑的调节涉及GABA能机制。
Several studies have provided evidence that suprapontine structures are involved in modulating the respiratory response to increases in carbon dioxide. However, the actual neuroanatomical site(s) responsible for this effect has not been identified. Therefore, the purpose of the present study was to determine if the posterior hypothalamus is one rostral site involved in the modulation of the respiratory response to hypercapnia. Phrenic nerve responses to progressive step increases in end-tidalPCO2were recorded before and after unilateral microinjection of γ-aminobutyric acid (GABA) antagonists into the posterior hypothalamus of anesthetized cats, which were paralyzed and ventilated. Microinjection of the antagonists reduced the apneic threshold to lower values of end-tidalPCO2. In addition, phrenic nerve responses to changes in CO2above the apneic threshold were augmented following microinjections of the GABA antagonists. This augmentation resulted from larger respiratory frequency responses with slight increases in the tidal phrenic response. Microinjection of a GABA agonist into the same hypothalamic site reversed the effects of the GABA antagonist. Microinjection of the GABA agonist without a preceding antagonist injection had no effects. These results suggest that the respiratory responses to increases inPCO2above the apneic threshold are modulated by neurons in the posterior hypothalamus in anesthetized cats. This hypothalamic modulation involves a GABAergic mechanism.