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

已经提出，在延髓头端腹外侧区中包括pFRG/Pre-I神经元的Phox 2b表达细胞作为中枢化学感受器（即CO2传感器）起作用。在本研究中，我们研究了高CO2接收的pFRG/前I神经元的神经机制，使用脑干脊髓制备从新生大鼠。pFRG/Pre-I神经元的CO2敏感性在Na+通道和Ca ~（2+）通道阻断后仍保持不变，高碳酸刺激引起的膜去极化主要是由于K ~+通道关闭所致。我们还发现，Phox 2b表达细胞，包括pFRG/前-I神经元在parfacial区域的头端腹侧延髓往往聚集在毛细血管周围。我们证实，TASK 1，2和3通道参与pFRG/Pre-I神经元的高碳酸反应不太明显。我们的研究结果表明，pFRG/Pre-I神经元具有突触后机制，直接负责高CO2刺激。

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.