Ionic mechanisms of CO2 sensitivity in Phox2b neurons as the medullary central chemoreceptor

已有研究表明，在延髓吻侧腹外侧区，PHOX2B表达的细胞包括pFRG/Pre-I神经元，其功能可能是中枢化学感受器(即CO2感受器)。在本研究中，我们使用新生大鼠的脑干-脊髓标本，研究了pFRG/Pre-I神经元高CO2接收的神经元机制。阻断Na~+通道和Ca~(2+)通道后，pFRG/Pre-I神经元对CO_2的敏感性仍保持不变，高碳酸血症引起的膜去极化主要是由于K~+通道关闭所致。我们还发现，包括pFRG/Pre-I神经元在内的PHOX2B表达细胞倾向于聚集在毛细血管周围。我们证实TASK1、2和3通道在pFRG/Pre-I神经元的高碳酸化反应中的作用较小。我们的发现表明，pFRG/Pre-I神经元具有直接与高二氧化碳刺激有关的突触后机制。

It has been suggested that Phox2b expressing cells including pFRG/Pre-I neurons in the rostral ventrolateral medulla function as the central chemoreceptors (i.e. CO2 sensor). In the present study, we investigated neuronal mechanisms of high CO2 reception of pFRG/Pre-I neurons, using the brainstem-spinal cord preparation from newborn rats. The CO2 sensitivity of pFRG/Pre-I neurons was preserved even after blockade of Na+channels and Ca2+channels, and the membrane depolarization induced by hypercapnic stimulation was mainly due to the closing of K+channels. We also found that Phox2b-expressing cells including pFRG/Pre-I neurons in the parafacial region of the rostral ventral medulla tended to assemble around capillary blood vessels. We confirmed that TASK1,2 and 3 channels were less significantly involved in hypercapnic responses of pFRG/Pre-I neurons. Our findings demonstrate that the pFRG/Pre-I neurons possess postsynaptic mechanisms that are directly responsible to high CO2 stimulation.