Li Yan-Chun, Wang Hui, Cao Ying, Tang Di, Wang Gui-Min, Yu Shu-Yan, Song Gang, Zhang Heng
Institute of Physiology, School of Medicine, Shandong University, Jinan 250012, China.
Sheng Li Xue Bao. 2005 Jun 25;57(3):395-9.
The aim of the present study was to observe whether protein tyrosine kinase (PTK) within the nucleus tractus solitarius (NTS) was involved in the regulation of ventilatory responses of peripheral chemoreflex. The experiments were performed on anesthetized, immobilized and artificially ventilated rabbits. Peripheral chemoreflex was elicited by ventilating the animal with 10% O2-balance 90% N2. Changes in the peak amplitude and frequency of integrated phrenic nerve activity were observed. The ventilatory responses of peripheral chemoreflex following 0.1 microl microinjection within the NTS of either PTK inhibitor genistein (10 mol/L), AMPA glutamate receptor inhibitor CNQX (10 mol/L),or inactive PTK inhibitor daidzein (10 mol/L) were recorded. The results are as follows: Both genistein and CNQX attenuated the ventilatory responses of peripheral chemoreflex, while no changes occurred following daidzein. The amplitude of integrated phrenic nerve discharge and the phrenic burst frequency were decreased by (-21.77+/-6.93)% and (-24.70+/-7.61)% respectively after administration of genistein. CNQX resulted in similar decreases in the amplitude of phrenic nerve discharge (-27.13+/-7.63)% and the burst frequency (-21.34+/-4.88)%. In addition, the inhibitory effects of CNQX and genistein were the same whether they were applied alone or one after another, indicating that they had no cooperative effects. The results obtained suggest that PTK within the NTS regulates the peripheral chemoreflex control of respiration and that this regulation of PTK may be mediated through the phosphorylation of AMPA receptors in NTS neurons.
本研究的目的是观察孤束核(NTS)内的蛋白酪氨酸激酶(PTK)是否参与外周化学反射通气反应的调节。实验在麻醉、固定并进行人工通气的家兔身上进行。通过用10% O₂平衡90% N₂对动物进行通气来引发外周化学反射。观察膈神经活动积分的峰值幅度和频率的变化。记录在NTS内微量注射0.1微升PTK抑制剂染料木黄酮(10微摩尔/升)、AMPA谷氨酸受体抑制剂CNQX(10微摩尔/升)或无活性的PTK抑制剂黄豆苷元(10微摩尔/升)后外周化学反射的通气反应。结果如下:染料木黄酮和CNQX均减弱了外周化学反射的通气反应,而黄豆苷元注射后未发生变化。注射染料木黄酮后,膈神经放电积分幅度和膈神经爆发频率分别降低了(-21.77±6.93)%和(-24.70±7.61)%。CNQX导致膈神经放电幅度(-27.13±7.63)%和爆发频率(-21.34±4.88)%出现类似程度的降低。此外,CNQX和染料木黄酮单独应用或先后应用时的抑制作用相同,表明它们没有协同作用。所得结果提示,NTS内的PTK调节呼吸的外周化学反射控制,且PTK的这种调节可能通过NTS神经元中AMPA受体的磷酸化介导。