ACTIONS OF DINITROPHENOL AND SOME OTHER METABOLIC INHIBITORS ON CORTICAL NEURONES
ACTIONS OF DINITROPHENOL AND SOME OTHER METABOLIC INHIBITORS ON CORTICAL NEURONES
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DOI：
10.1113/jphysiol.1971.sp009465
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发表时间：
1971-01-01
影响因子：
5.5
通讯作者：
PUMAIN, R
中科院分区：
文献类型：
--
作者：
GODFRAIND, JM;KAWAMURA, H;PUMAIN, R
1.在猫下甲氧氟烷，DNP和其他代谢抑制剂进行了测试，皮质神经元的离子电渗从微量移液器。2.二硝基苯酚，二硝基邻甲酚，碘乙酸，五氯苯酚和寡霉素（解偶联剂或氧化磷酸化抑制剂），以及中度缺氧，选择性和可逆性阻断自发放电和放电引起的乙酰胆碱引起的谷氨酸引起的反应，促进由中等剂量的二硝基苯酚和阻断只有大量。3.叠氮化物，氰化物，哇巴因和毒毛旋花子碱主要有兴奋作用;强心苷往往抑制更强烈的反应谷氨酸。4.细胞内观察表明，DNP导致电兴奋性急剧下降，与超极化和膜电阻下降。5. DNP的超极化作用的平均逆转水平（EDNP）比静息电位负近30 mV; EDNP与ACh去极化作用的平均逆转水平相同，在相同的细胞上测量。6. DNP对IPSP通过提高内部[Cl]而呈阳性的神经元有其通常的超极化作用;平均EIPSP比EDNP阳性超过30 mV。7.它的结论是，DNP降低兴奋性，通过提高膜电导K+（GK），它选择性地阻断ACh反应，因为ACh对这些神经元有一个完全相反的行动。8.在讨论中，有人建议，gK的上升是介导的内部游离Ca 2+的增加，引起线粒体活性的减缓，并且类似的机制可能在全身麻醉中发挥重要作用。
1. In cats under methoxyflurane, DNP and other metabolic inhibitors were tested on cortical neurones by iontophoresis from micropipettes. 2. DNP, dinitro-o-cresol, iodoacetate, pentachlorophenol and oligomycin (uncouplers or inhibitors of oxidative phosphorylation), as well as moderate anoxia, blocked selectively and reversibly spontaneous firing and discharges evoked by ACh; responses evoked by glutamate were facilitated by moderate doses of DNP and blocked only by large amounts. 3. Azide, cyanide, ouabain and strophanthidine had a mainly excitatory effect; the cardiac glycosides tended to depress more strongly responses to glutamate. 4. Intracellular observations showed that DNP causes a sharp fall in electrical excitability, associated with a hyperpolarization and fall in membrane resistance. 5. The hyperpolarizing action of DNP had a mean reversal level (EDNP) nearly 30 mV more negative than the resting potential; EDNP was identical with the mean reversal level for the depolarizing action of ACh, measured on the same cells. 6. DNP had its usual hyperpolarizing effect on neurones whose IPSPs had been made positive by raising the internal [Cl]; the mean EIPSP was over 30 mV more positive than EDNP. 7. It is concluded that DNP lowers excitability by raising the membrane conductance to K+ (gK) and that it blocks ACh responses selectively because ACh has a precisely opposite action on these neurones. 8. In the Discussion, it is suggested that the rise in gK is mediated by an increase in internal free Ca2+, caused by a slowing of mitochondrial activity, and that a similar mechanism may play a significant role in general anaesthesia.