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本文引用的文献

1
Synaptic acidification enhances GABAA signaling.突触酸化增强 GABA 信号转导。
J Neurosci. 2010 Nov 24;30(47):16044-52. doi: 10.1523/JNEUROSCI.6364-09.2010.
2
Acid-sensitive ion channels and receptors.酸敏感离子通道与受体。
Handb Exp Pharmacol. 2009(194):283-332. doi: 10.1007/978-3-540-79090-7_9.
3
Motor deficit in a Drosophila model of mucolipidosis type IV due to defective clearance of apoptotic cells.由于凋亡细胞清除缺陷导致的IV型粘脂贮积症果蝇模型中的运动功能障碍。
Cell. 2008 Nov 28;135(5):838-51. doi: 10.1016/j.cell.2008.09.041.
4
Bioenergetics of cerebral ischemia: a cellular perspective.脑缺血的生物能量学:细胞层面的视角
Neuropharmacology. 2008 Sep;55(3):289-309. doi: 10.1016/j.neuropharm.2008.05.023. Epub 2008 Jun 3.
5
Local extracellular acidification caused by Ca2+-dependent exocytosis in PC12 cells.PC12细胞中由Ca2+依赖性胞吐作用引起的局部细胞外酸化。
Cell Calcium. 2008 Aug;44(2):220-9. doi: 10.1016/j.ceca.2007.12.003. Epub 2008 Mar 17.
6
Isoflurane reduces excitability of Drosophila larval motoneurons by activating a hyperpolarizing leak conductance.异氟烷通过激活超极化漏电导降低果蝇幼虫运动神经元的兴奋性。
Anesthesiology. 2008 Mar;108(3):434-46. doi: 10.1097/ALN.0b013e318164cfda.
7
Acid-sensing ion channels interact with and inhibit BK K+ channels.酸敏感离子通道与BK钾通道相互作用并抑制后者。
Proc Natl Acad Sci U S A. 2008 Feb 26;105(8):3140-4. doi: 10.1073/pnas.0712280105. Epub 2008 Feb 14.
8
Extracellular pH modulates the voltage-dependent Ca2+ current and low threshold K+ current in hair cells.细胞外pH值调节毛细胞中电压依赖性Ca2+电流和低阈值K+电流。
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10
Novel Drosophila two-pore domain K channels: rescue of channel function by heteromeric assembly.新型果蝇双孔结构域钾通道:通过异源组装挽救通道功能。
Eur J Neurosci. 2006 Oct;24(8):2264-74. doi: 10.1111/j.1460-9568.2006.05102.x.

细胞外质子会降低果蝇幼虫神经肌肉接头处的量子含量并延长突触电流。

Extracellular protons reduce quantal content and prolong synaptic currents at the Drosophila larval neuromuscular junction.

作者信息

Sandstrom David J

机构信息

Laboratory of Molecular Biology, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892, USA.

出版信息

J Neurogenet. 2011 Oct;25(3):104-14. doi: 10.3109/01677063.2011.606577. Epub 2011 Aug 30.

DOI:10.3109/01677063.2011.606577
PMID:21877902
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3462067/
Abstract

Fluctuations in extracellular pH occur in the nervous system in response to a number of physiological and pathological processes, such as ischemia, hypercapnea, and high-frequency activity. Using the Drosophila larval neuromuscular junction, the author has examined acute effects of low and high pH on excitability and synaptic transmission. Acidification rapidly and reversibly reduces the size of electrically evoked excitatory junctional currents (EJCs) in a concentration-dependent manner, with transmission nearly abolished at pH 5.0. Conversely, raising pH to 7.8 increases EJC amplitude significantly. Further elevation to pH 8.5 causes an initial increase in amplitude, followed by profound, long-lasting depression of the synapse. Amplitudes of spontaneous miniature EJCs (mEJCs) are modestly, but significantly reduced at pH 5.0. It is therefore the number of quanta released per action potential, rather than the size of individual quanta, that is most strongly affected. Decay times of both EJCs and mEJCs are dramatically lengthened at low pH, suggesting that glutamate remains in the synaptic cleft for much longer than normal. Presynaptic excitability is also reduced, as indicated by increased latency between nerve shock and EJC onset. The response to low pH was not altered by mutations in genes encoding Transient Receptor Potential, Mucolipin subfamily (TRPML) and Slowpoke ion channels, which had previously been implicated as possible targets of extracellular protons. The author concludes that extracellular protons have strong effects on the release of glutamate and the time course of synaptic currents. These phenotypes can be exploited to study the mechanisms of acid-mediated changes in neuronal function, and to pursue the way in which pH modulates synaptic function in normal and pathophysiological conditions.

摘要

细胞外pH值的波动会在神经系统中因多种生理和病理过程而出现,如局部缺血、高碳酸血症和高频活动。利用果蝇幼虫神经肌肉接头,作者研究了低pH值和高pH值对兴奋性和突触传递的急性影响。酸化以浓度依赖的方式迅速且可逆地降低电诱发兴奋性接头电流(EJC)的大小,在pH 5.0时传递几乎完全消失。相反,将pH值提高到7.8会显著增加EJC幅度。进一步提高到pH 8.5会导致幅度最初增加,随后是突触的深度、持久抑制。自发微小EJC(mEJC)的幅度在pH 5.0时适度但显著降低。因此,每个动作电位释放的量子数受到的影响最为强烈,而不是单个量子的大小。在低pH值时,EJC和mEJC的衰减时间都显著延长,这表明谷氨酸在突触间隙中停留的时间比正常情况长得多。突触前兴奋性也降低,这表现为神经冲击与EJC开始之间的潜伏期增加。编码瞬时受体电位、黏液脂蛋白亚家族(TRPML)和慢poke离子通道的基因突变并未改变对低pH值的反应,这些基因以前被认为可能是细胞外质子的作用靶点。作者得出结论,细胞外质子对谷氨酸的释放和突触电流的时间进程有强烈影响。这些表型可用于研究酸介导的神经元功能变化机制,并探索pH值在正常和病理生理条件下调节突触功能的确切方式。