Takeda Mamoru, Matsumoto Shigeji
Department of Physiology, Nippon Dental University, School of Dentistry at Tokyo, 1-9-20, Fujimi-cho, Chiyoda-ku, Japan.
Life Sci. 2002 Oct 18;71(22):2681-90. doi: 10.1016/s0024-3205(02)02101-x.
To clarify whether GABAergic or glycinergic transmission alters the activity of inspiratory neurons during spontaneous augmented breaths, we recorded the single unit activity from inspiratory neurons in the dorsal and ventral respiratory groups in the medulla of pentobarbital anesthetized rats and applied GABA(A) and glycine receptor agonists by iontophoresis using multibarrel microelectrodes. The spontaneous augmented breath was divided into two different phases; the first phase (phase I) resembled a normal inspiration but the second phase (phase II) indicated a marked increase in diaphragm electromyogram activity. During application of either muscimol or glycine, the discharge of inspiratory neurons during the phase I of spontaneous augmented breaths was suppressed, but the augmenting discharge of the phase II did not change significantly in any cell type of the neurons (I-augmenting, I-decrementing and I-other). These results suggested that the excitatory inputs to inspiratory neurons during the phase II of augmented breaths may not be significantly influenced by the activation of either GABA(A) receptors or glycine receptors.
为了阐明在自发性增强呼吸过程中，γ-氨基丁酸能（GABAergic）或甘氨酸能（glycinergic）传递是否会改变吸气神经元的活动，我们记录了戊巴比妥麻醉大鼠延髓背侧和腹侧呼吸组中吸气神经元的单单位活动，并使用多管微电极通过离子电泳施加GABA(A)和甘氨酸受体激动剂。自发性增强呼吸分为两个不同阶段；第一阶段（阶段I）类似于正常吸气，但第二阶段（阶段II）表明膈肌肌电图活动显著增加。在应用蝇蕈醇或甘氨酸期间，自发性增强呼吸阶段I期间吸气神经元的放电受到抑制，但阶段II的增强放电在任何神经元细胞类型（I型增强、I型递减和I型其他）中均无显著变化。这些结果表明，增强呼吸阶段II期间吸气神经元的兴奋性输入可能不会受到GABA(A)受体或甘氨酸受体激活的显著影响。
