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二氧化碳对孤束核中神经元的去极化和刺激并不需要化学突触输入。

Depolarization and stimulation of neurons in nucleus tractus solitarii by carbon dioxide does not require chemical synaptic input.

作者信息

Dean J B, Bayliss D A, Erickson J T, Lawing W L, Millhorn D E

机构信息

Department of Physiology, University of North Carolina, Chapel Hill 27599.

出版信息

Neuroscience. 1990;36(1):207-16. doi: 10.1016/0306-4522(90)90363-9.

DOI:10.1016/0306-4522(90)90363-9
PMID:2120613
Abstract

The effects of elevated CO2 (i.e. hypercapnia) on neurons in the nucleus tractus solitarii were studied using extracellular (n = 82) and intracellular (n = 33) recording techniques in transverse brain slices prepared from rat. Synaptic connections from putative chemosensitive neurons in the ventrolateral medulla were removed by bisecting each transverse slice and discarding the ventral half. In addition, the response to hypercapnia in 20 neurons was studied during high magnesium-low calcium synaptic blockade. Sixty-five per cent of the neurons (n = 75) tested were either insensitive or inhibited by hypercapnia. However, 35% (n = 40) were depolarized and/or increased their firing rate during hypercapnia. Nine out of 10 CO2-excited neurons retained their chemosensitivity to CO2 in the presence of high magnesium-low calcium synaptic blockade medium. Our findings demonstrate that many neurons in the nucleus tractus solitarii were depolarized and/or increased their firing rate during hypercapnia. These neurons were not driven synaptically by putative chemosensitive neurons of the ventrolateral medulla since this region was removed from the slice. Furthermore, because chemosensitivity persisted in most neurons tested during synaptic blockade, we conclude that some neurons in the nucleus tractus solitarii are inherently CO2-chemosensitive. Although the function of dorsal medullary chemosensitive neurons cannot be determined in vitro, their location and their inherent chemosensitivity suggest a role in cardiorespiratory central chemoreception.

摘要

利用细胞外记录技术(n = 82)和细胞内记录技术(n = 33),在大鼠制备的横断脑片中研究了高二氧化碳(即高碳酸血症)对孤束核神经元的影响。通过将每个横断切片一分为二并丢弃腹侧一半,去除了来自延髓腹外侧假定化学敏感神经元的突触连接。此外,在高镁 - 低钙突触阻断期间研究了20个神经元对高碳酸血症的反应。所测试的65%的神经元(n = 75)对高碳酸血症不敏感或受到抑制。然而,35%(n = 40)在高碳酸血症期间发生去极化和/或增加其放电频率。在高镁 - 低钙突触阻断介质存在的情况下,10个二氧化碳兴奋的神经元中有9个保留了对二氧化碳的化学敏感性。我们的研究结果表明,许多孤束核神经元在高碳酸血症期间发生去极化和/或增加其放电频率。这些神经元不是由延髓腹外侧假定化学敏感神经元通过突触驱动的,因为该区域已从切片中去除。此外,由于在突触阻断期间大多数测试神经元的化学敏感性持续存在,我们得出结论,孤束核中的一些神经元具有内在的二氧化碳化学敏感性。虽然延髓背侧化学敏感神经元的功能无法在体外确定,但其位置和内在化学敏感性表明其在心肺中枢化学感受中起作用。

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