Dillon G H, Waldrop T G
Department of Physiology and Biophysics, University of Illinois, Urbana 61801.
Neuroscience. 1992 Dec;51(4):941-50. doi: 10.1016/0306-4522(92)90531-6.
Results from previous studies have suggested that the hypothalamus modulates cardiorespiratory responses to hypoxia and/or hypercapnia. Many neurons in the caudal hypothalamus are stimulated by hypercapnia and hypoxia in vivo; however, it is not known if these responses are dependent upon input from other areas. Whole-cell patch and extracellular recordings from a brain slice preparation were used in the present study to determine the direct effects of hypoxia (5% CO2/95% N2 or 10% O2/5% CO2/85% N2) and hypercapnia (7% CO2/93% O2) on caudal hypothalamic neurons in vitro. Coronal sections (400-500 microns) were obtained from young Sprague-Dawley rats and placed in a recording chamber that was perfused with nutrient media equilibrated with 95% O2/5% CO2. Extracellular recordings demonstrated that hypoxia stimulated over 80% of the neurons tested; the magnitude of the response was dependent upon the degree of hypoxia. In addition, over 80% of cells that were excited by hypoxia retained this response during synaptic blockade. Hypercapnia increased the discharge frequency of 22% of the caudal hypothalamic neurons that were studied. A second set of caudal hypothalamic neurons were studied with whole-cell patch recordings; the mean resting membrane potential of these neurons was -51.8 +/- 1.0 mV with an average input resistance of 399 +/- 49 M omega. Hypoxia produced a depolarization in 76% of these neurons; a poststimulus hyperpolarization often occurred. A depolarization and/or increase in discharge rate during hypercapnia was observed in 35% of the neurons tested. Only 10% of all neurons studied were excited by both hypoxia and hypercapnia. These findings suggest that separate subpopulations of caudal hypothalamic neurons are sensitive to hypoxia and hypercapnia. Thus, this hypothalamic area may be a site of central hypoxic and hypercapnic chemoreception.
以往研究结果表明，下丘脑可调节机体对低氧和/或高碳酸血症的心肺反应。在活体中，下丘脑尾部的许多神经元会受到高碳酸血症和低氧的刺激；然而，尚不清楚这些反应是否依赖于其他区域的输入。在本研究中，我们采用脑片制备的全细胞膜片钳和细胞外记录技术，来确定低氧（5%二氧化碳/95%氮气或10%氧气/5%二氧化碳/85%氮气）和高碳酸血症（7%二氧化碳/93%氧气）对体外下丘脑尾部神经元的直接影响。从幼年Sprague-Dawley大鼠获取冠状切片（400 - 500微米），并将其置于充满用95%氧气/5%二氧化碳平衡的营养培养基灌注的记录室中。细胞外记录表明，低氧刺激了超过80%的受试神经元；反应的幅度取决于低氧的程度。此外，超过80%受低氧兴奋的细胞在突触阻断期间仍保留该反应。高碳酸血症使所研究的下丘脑尾部神经元中22%的放电频率增加。另一组下丘脑尾部神经元采用全细胞膜片钳记录进行研究；这些神经元的平均静息膜电位为-51.8±1.0毫伏，平均输入电阻为399±49兆欧。低氧使这些神经元中的76%产生去极化；刺激后常出现超极化。在35%的受试神经元中观察到高碳酸血症期间的去极化和/或放电率增加。所有研究的神经元中只有10%同时受到低氧和高碳酸血症的兴奋。这些发现表明，下丘脑尾部神经元的不同亚群对低氧和高碳酸血症敏感。因此，该下丘脑区域可能是中枢性低氧和高碳酸血症化学感受的部位。
