【摘要】 本工作旨在观察脑干孤束核内蛋白酪氨酸激酶(proteintyrosinekinase,PTK)是否参与了外周化学感受性反射的呼吸反应调节。实验采用电生理和微量注射相结合的方法,以膈神经放电为观察指标,观察呼吸变化。通过吸入10%氧气(10%O2,90%N2)引导出外周化学感受性反射。在孤束核(nucleustractussolitarius,NTS)处分别微量注射蛋白酪氨酸激酶的抑制剂genistein和其非活动性抑制剂daidzein以及AMPA受体阻断剂CNQX,观察这些药物对外周化学感受性反射的影响。结果显示,吸入低氧混合气后,动物呼吸加深加快;在NTS处微量注射CNQX或genistein都会不同程度削弱外周化学感受性反射引起的通气反应,而微量注射daidzein后对反射没有影响。另外,在NTS处微量注射CNQX后再注射genistein,其削弱外周化学感受性反射的作用与单独微量注射CNQX或genistein基本相同,二者并无协同作用。结果提示,NTS处的蛋白酪氨酸激酶对外周化学感受性反射具有一定的调节作用,并且NTS处磷酸化修饰AMPA受体可能是PTK发挥这种调节作用的途径之一。更多还原

【Abstract】 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 ofperipheral chemoreflex following 0.1 μl microinjection within the NTS of either PTK inhibitor genistein(10 mol/L), AMPA glutamatereceptor inhibitor CNQX (10 mol/L),or inactive PTK inhibitor daidzein (10 mol/L) were recorded. The results are as follows: Bothgenistein 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 samewhether they were applied alone or one after another, indicating that they had no cooperative effects. The results obtained suggest thatPTK within the NTS regulates the peripheral chemoreflex control of respiration and that this regulation of PTK may be mediatedthrough the phosphorylation of AMPA receptors in NTS neurons.更多还原