Synaptic physiology and mitochondrial function in crayfish tonic and phasic motor neurons
Synaptic physiology and mitochondrial function in crayfish tonic and phasic motor neurons
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DOI：
10.1152/jn.1997.78.1.281
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发表时间：
1997-07-01
影响因子：
2.5
通讯作者：
Atwood, HL
中科院分区：
文献类型：
--
作者：
Nguyen, PV;Marin, L;Atwood, HL
甲壳类动物的时相运动神经元和强直运动神经元在连接突触生理学上有显著的不同。紧张性神经元通常产生小的兴奋性突触后电位（EPSP），其随着刺激频率的增加而强烈地促进，并且通常不显示突触抑制。相比之下，时相神经元产生相对较大的EPSP，具有较弱的频率易化和明显的抑制。我们提出了线粒体功能是这些神经元突触传递特征的重要决定因素的假设。线粒体荧光共聚焦显微镜测量后，暴露于超活体线粒体荧光染料，罗丹明-123（Rh 123）和4-二乙氨基苯乙烯基-N-甲基吡啶碘（4-Di-2-Asp）的阶段性和紧张性轴突和终端的腹部和腿部肌肉。强直性轴突和神经肌肉接头的线粒体有显着较高的平均Rh 123和4-Di-2-Asp荧光比相位神经元，表明更多的积累的荧光染料。线粒体膜电位，这是负责Rh 123的摄取，并与线粒体氧化活性（代谢底物的氧化产生ATP），可能是更高的紧张性轴突。电子显微镜显示，强直性轴突每μ m（2）横截面积包含的线粒体大约是相位性轴突的5倍。紧张性轴突的神经肌肉接头也比相位性轴突具有高得多的线粒体含量。我们测试的假设，突触疲劳的阻力是依赖于线粒体功能的小龙虾运动轴突。氧化磷酸化解偶联剂，二硝基苯酚或羰基氰间氯苯腙，或电子传递抑制剂叠氮化钠，线粒体功能受损，导致显着的突触抑制的紧张性轴突和加速抑郁症的阶段性轴突在维持刺激。碘乙酸，糖酵解抑制剂，氯霉素，线粒体蛋白质合成抑制剂，无论是线粒体荧光或突触抑制紧张性或阶段性轴突没有显着的影响。总的来说，结果提供的证据表明，线粒体氧化代谢是重要的，在维持刺激的紧张性和相位运动神经元的突触传递。紧张性神经元具有更高的线粒体含量和更大的氧化活性;这些特征与它们对突触抑制的更大抵抗力相关。相反，相位神经元具有较低的线粒体含量，较少的氧化活性和较大的突触疲劳性。
Phasic and tonic motor neurons of crustaceans differ strikingly in their junctional synaptic physiology. Tonic neurons generally produce small excitatory postsynaptic potentials (EPSPs) that facilitate strongly as stimulation frequency is increased, and normally show no synaptic depression. In contrast, phasic neurons produce relatively large EPSPs with weak frequency facilitation and pronounced depression. We addressed the hypothesis that mitochondrial function is an important determinant of the features of synaptic transmission in these neurons. Mitochondrial fluorescence was measured with confocal microscopy in phasic and tonic axons and terminals of abdominal and leg muscles after exposure to supravital mitochondrial fluorochromes, rhodamine-123 (Rh123) and 4-diethylaminostyryl-N-methylpyridinium iodide (4-Di-2-Asp). Mitochondria of tonic axons and neuromuscular junctions had significantly higher mean Rh123 and 4-Di-2-Asp fluorescence than in phasic neurons, indicating more accumulation of the fluorochromes. Mitochondrial membrane potential, which is responsible for Rh123 uptake and is related to mitochondrial oxidative activity (the production of ATP by oxidation of metabolic substrates), is likely higher in tonic axons. Electron microscopy showed that tonic axons contain approximately fivefold more mitochondria per mu m(2) cross-sectional area than phasic axons. Neuromuscular junctions of tonic axons also have a much higher mitochondrial content than those of phasic axons. We tested the hypothesis that synaptic fatigue resistance is dependent on mitochondrial function in crayfish motor axons. Impairment of mitochondrial function by uncouplers of oxidative phosphorylation, dinitrophenol or carbonyl cyanide m-chlorophenylhydrazone, or by the electron transport inhibitor sodium azide, led to marked synaptic depression of a tonic axon and accelerated depression of a phasic axon during maintained stimulation. Iodoacetate, an inhibitor of glycolysis, and chloramphenicol, a mitochondrial protein synthesis inhibitor, had no significant effects on either mitochondrial fluorescence or synaptic depression in tonic or phasic axons. Collectively, the results provide evidence that mitochondrial oxidative metabolism is important for sustaining synaptic transmission during maintained stimulation of tonic and phasic motor neurons. Tonic neurons have a higher mitochondrial content and greater oxidative activity; these features are correlated with their greater resistance to synaptic depression. Conversely, phasic neurons have a lower mitochondrial content, less oxidative activity, and greater synaptic fatigability.