ENERGY-METABOLISM IN RAT-BRAIN SYNAPTOSOMES FROM NEMBUTAL-ANESTHETIZED AND NON-ANESTHETIZED ANIMALS
ENERGY-METABOLISM IN RAT-BRAIN SYNAPTOSOMES FROM NEMBUTAL-ANESTHETIZED AND NON-ANESTHETIZED ANIMALS
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DOI：
10.1111/j.1471-4159.1980.tb11218.x
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发表时间：
1980-01-01
影响因子：
4.7
通讯作者：
WILSON, DF
中科院分区：
文献类型：
--
作者：
RAFALOWSKA, U;ERECINSKA, M;WILSON, DF
研究了麻醉和非麻醉大鼠脑突触体悬浮液中线粒体内和胞质内[NAD+]/[NADH]比值、细胞内[ATP]/[ADP][Pi]和[磷酸肌酸]/[肌酸]比值、细胞色素c浓度及其氧化还原状态和呼吸速率等细胞能量参数。未麻醉大鼠突触体中[3-羟基丁酸酯]与[乙酰乙酸酯]的比值为2.0，麻醉动物突触体中[3-羟基丁酸酯]与[乙酰乙酸酯]的比值为5.55。前者的[乳酸]/[丙酮酸]比值为3.8，后者的[乳酸]/[丙酮酸]比值为10.9。麻醉大鼠突触体的[ATP]/[ADP][Pi]分别为3838 M和840 M，[磷酸肌酸]/[肌酸]比值分别为0.79和0.39。细胞色素c在两种制剂中均降低约15%；非麻醉动物突触体的线粒体细胞色素浓度几乎高出2倍。线粒体氧化还原反应与ATP合成之间的自由能关系表明，在麻醉大鼠脑内分离的突触体中，氧化磷酸化的前2个位点处于接近平衡状态，与完整的细胞和组织相对应。麻醉大鼠突触体的能量参数与完整全脑的能量参数非常相似。未麻醉大鼠的突触体则较低。在隔离期间，戊巴坦麻醉显然可以防止对突触体的一些不可逆损伤。从麻醉大鼠脑内分离的突触体显然可以作为研究神经元代谢的一个方便的模型系统。
Cellular energetic parameters including the intramitochondria and cytosolic [NAD+]/[NADH] ratios, the cellular [ATP]/[ADP][Pi] and [creatine phosphate]/[creatine] ratios, the concentration of cytochrome c and its redox state, and the respiratory rate were studied in suspensions of rat brain synaptosomes isolated from nembutal-anesthetized and nonanesthetized animals. The ratio of [3-hydroxybutyrate] to [acetoacetate] was 2.0 in synaptosomes isolated from nonanesthetized rats and 5.55 in those from anesthetized animals. The [lactate]/[pyruvate] ratio was 3.8 in the former and 10.9 in the latter preparation. The [ATP]/[ADP][Pi] was 3838 M in the synaptosomes from anesthetized rats and 840 M in those from nonanesthetized animals: the [creatine phosphate]/[creatine] ratios were 0.79 and 0.39, respectively. Cytochrome c was about 15% reduced in both preparations; the mitochondrial cytochrome concentration was almost 2-fold higher in the synaptosomes from nonanesthetized animals. The free energy relationships between the mitochondrial redox reactions and ATP synthesis showed that in synaptosomes isolated from the brains of nembutal-anesthetized rats the first 2 sites of oxidative phosphorylation were at near-equilibrium, corresponding to intact cells and tissues. The energetic parameters for synaptosomes from anesthetized rats are very similar to the values for intact whole brain. Those for synaptosomes from nonanesthetized rats are lower. Nembutal anesthesia apparently protects against some irreversible damage to the synaptosome during isolation. Synaptosomes isolated from brains of nembutal-anesthetized rats apparently can be used as a convenient model system for studies of neuronal metabolism.