Lawson E E, Richter D W, Ballantyne D, Lalley P M
I. Physiologisches Institut der Universität Heidelberg, Federal Republic of Germany.
Pflugers Arch. 1989 Sep;414(5):523-33. doi: 10.1007/BF00580987.
The effect of peripheral chemoreceptor activation on inspiratory and postinspiratory medullary neurons was investigated using intracellular recording techniques. Peripheral chemoreceptors were activated by injecting CO2 saturated 1 N bicarbonate solution into the lingual artery or by electrically stimulating the carotid sinus nerve. Injections of 20-300 microliters bicarbonate solution evoked changes in respiratory frequency and in peak phrenic nerve discharge. The membrane potential of inspiratory alpha neurons, whether bulbospinal or not and independent of their anatomic location, was decreased during inspiration. A sequence of compound excitatory and inhibitory effects were observed when the stimulus was given during the postinspiratory and expiratory phases of the respiratory cycle. Inspiratory beta- and late-inspiratory neurons, however, were inhibited by peripheral chemoreceptor activation. Postinspiratory neurons were strongly activated during postinspiration. Neither class of respiratory neurons were shown to receive direct synaptic inputs from the peripheral chemoreceptors as tested by electrical stimulation of the carotid sinus nerve and signal averaging of the respiratory neuron membrane potential. The experiments revealed differential influences of afferent chemoreceptor activity on various components of the respiratory network. We conclude that chemoreceptor afferents activate non-respiratory modulated medullary neurons which, in turn, activate or inhibit various neurons of the medullary respiratory control network. The responses of each type of respiratory neuron to chemoreceptors afferents may then be considered in the context of this direct interaction as well as the network interactions of the various cells.
利用细胞内记录技术,研究了外周化学感受器激活对吸气和吸气后延髓神经元的影响。通过向舌动脉注射二氧化碳饱和的1N碳酸氢盐溶液或电刺激颈动脉窦神经来激活外周化学感受器。注射20 - 300微升碳酸氢盐溶液可引起呼吸频率和膈神经放电峰值的变化。吸气性α神经元的膜电位,无论是否为延髓脊髓性且与其解剖位置无关,在吸气时都会降低。当在呼吸周期的吸气后和呼气阶段给予刺激时,观察到一系列复合的兴奋和抑制作用。然而,吸气性β神经元和晚吸气神经元会被外周化学感受器激活所抑制。吸气后神经元在吸气后强烈激活。通过电刺激颈动脉窦神经和对呼吸神经元膜电位进行信号平均测试,未发现这两类呼吸神经元接受来自外周化学感受器的直接突触输入。实验揭示了传入化学感受器活动对呼吸网络各组成部分的不同影响。我们得出结论,化学感受器传入神经激活非呼吸调制的延髓神经元,进而激活或抑制延髓呼吸控制网络的各种神经元。然后,在这种直接相互作用以及各种细胞的网络相互作用的背景下,可以考虑每种类型的呼吸神经元对化学感受器传入神经的反应。