钙离子诱导的γ-氨基丁酸介导电流的反弹增强需要Ca2+/钙调蛋白依赖性激酶II的激活。
Ca(2+)-induced rebound potentiation of gamma-aminobutyric acid-mediated currents requires activation of Ca2+/calmodulin-dependent kinase II.
作者信息
Kano M, Kano M, Fukunaga K, Konnerth A
机构信息
Department of Physiology, Jichi Medical School, Tochigi, Japan.
出版信息
Proc Natl Acad Sci U S A. 1996 Nov 12;93(23):13351-6. doi: 10.1073/pnas.93.23.13351.
Abstract
In cerebellar Purkinje neurons, gamma-aminobutyric acid (GABA)-mediated inhibitory synaptic transmission undergoes a long-lasting "rebound potentiation" after the activation of excitatory climbing fiber inputs. Rebound potentiation is triggered by the climbing-fiber-induced transient elevation of intracellular Ca2+ concentration and is expressed as a long-lasting increase of postsynaptic GABAA receptor sensitivity. Herein we show that inhibitors of the Ca2+/calmodulin-dependent protein kinase II (CaM-KII) signal transduction pathway effectively block the induction of rebound potentiation. These inhibitors have no effect on the once established rebound potentiation, on voltage-gated Ca2+ channel currents, or on the basal inhibitory transmission itself. Furthermore, a protein phosphatase inhibitor and the intracellularly applied CaM-KII markedly enhanced GABA-mediated currents in Purkinje neurons. Our results demonstrate that CaM-KII activation and the following phosphorylation are key steps for rebound potentiation.
摘要
在小脑浦肯野神经元中，兴奋性攀缘纤维输入激活后，γ-氨基丁酸（GABA）介导的抑制性突触传递会经历持久的“反弹增强”。反弹增强由攀缘纤维诱导的细胞内Ca2+浓度瞬时升高触发，并表现为突触后GABAA受体敏感性的持久增加。在此我们表明，Ca2+/钙调蛋白依赖性蛋白激酶II（CaM-KII）信号转导途径的抑制剂可有效阻断反弹增强的诱导。这些抑制剂对一旦建立的反弹增强、电压门控Ca2+通道电流或基础抑制性传递本身均无影响。此外，一种蛋白磷酸酶抑制剂和细胞内应用的CaM-KII显著增强了浦肯野神经元中GABA介导的电流。我们的结果表明，CaM-KII的激活及随后的磷酸化是反弹增强的关键步骤。
相似文献
1
Ca(2+)-induced rebound potentiation of gamma-aminobutyric acid-mediated currents requires activation of Ca2+/calmodulin-dependent kinase II.钙离子诱导的γ-氨基丁酸介导电流的反弹增强需要Ca2+/钙调蛋白依赖性激酶II的激活。
Proc Natl Acad Sci U S A. 1996 Nov 12;93(23):13351-6. doi: 10.1073/pnas.93.23.13351.
2
Synaptic excitation produces a long-lasting rebound potentiation of inhibitory synaptic signals in cerebellar Purkinje cells.突触兴奋在小脑浦肯野细胞中产生抑制性突触信号的持久反弹增强。
Nature. 1992 Apr 16;356(6370):601-4. doi: 10.1038/356601a0.
3
Signaling cascade regulating long-term potentiation of GABA(A) receptor responsiveness in cerebellar Purkinje neurons.调节小脑浦肯野神经元中GABA(A)受体反应性长期增强的信号级联反应。
J Neurosci. 2002 May 15;22(10):3969-76. doi: 10.1523/JNEUROSCI.22-10-03969.2002.
4
Differential Modulation of GABAA Receptors Underlies Postsynaptic Depolarization- and Purinoceptor-Mediated Enhancement of Cerebellar Inhibitory Transmission: A Non-Stationary Fluctuation Analysis Study.GABAA受体的差异调节是突触后去极化和嘌呤能受体介导的小脑抑制性传递增强的基础：一项非平稳波动分析研究。
PLoS One. 2016 Mar 1;11(3):e0150636. doi: 10.1371/journal.pone.0150636. eCollection 2016.
5
Regulatory phosphorylation of AMPA-type glutamate receptors by CaM-KII during long-term potentiation.在长时程增强过程中，CaM-KII对AMPA型谷氨酸受体的调节性磷酸化作用。
Science. 1997 Jun 27;276(5321):2042-5. doi: 10.1126/science.276.5321.2042.
6
Regulation of synaptic facilitation by postsynaptic Ca2+/CaM pathways in hippocampal CA1 neurons.海马体CA1神经元中突触后Ca2+/钙调蛋白途径对突触易化的调节作用。
J Neurophysiol. 1996 Jul;76(1):276-86. doi: 10.1152/jn.1996.76.1.276.
7
Modulation of glutamate sensitivities by inhibitors of a protein kinase and a protein phosphatase in cultured rat Purkinje cells.蛋白激酶和蛋白磷酸酶抑制剂对培养大鼠浦肯野细胞谷氨酸敏感性的调节作用。
Neurosci Lett. 1998 May 15;247(2-3):139-42. doi: 10.1016/s0304-3940(98)00299-7.
8
Monoaminergic long-term facilitation of GABA-mediated inhibitory transmission at cerebellar synapses.小脑突触处GABA介导的抑制性突触传递的单胺能长期易化作用。
Neuroscience. 1999;88(3):871-83. doi: 10.1016/s0306-4522(98)00260-7.
9
Potentiation of GABA-mediated currents by cAMP-dependent protein kinase.环磷酸腺苷（cAMP）依赖性蛋白激酶对γ-氨基丁酸（GABA）介导电流的增强作用。
Neuroreport. 1992 Jul;3(7):563-6. doi: 10.1097/00001756-199207000-00004.
10
Evidence for protein tyrosine phosphatase, tyrosine kinase, and G-protein regulation of the parallel fiber metabotropic slow EPSC of rat cerebellar Purkinje neurons.大鼠小脑浦肯野神经元平行纤维代谢型慢兴奋性突触后电流的蛋白酪氨酸磷酸酶、酪氨酸激酶及G蛋白调节的证据
J Neurosci. 2003 May 15;23(10):4066-71. doi: 10.1523/JNEUROSCI.23-10-04066.2003.
引用本文的文献
1
Morphological and Functional Principles Governing the Plasticity Reserve in the Cerebellum: The Cortico-Deep Cerebellar Nuclei Loop Model.小脑可塑性储备的形态学和功能原理：皮质-深部小脑核团环路模型
Biology (Basel). 2023 Nov 16;12(11):1435. doi: 10.3390/biology12111435.
2
UNC-43/CaMKII-triggered anterograde signals recruit GABARs to mediate inhibitory synaptic transmission and plasticity at C. elegans NMJs.UNC-43/CaMKII 触发的顺行信号募集 GABAARs 介导线虫 NMJs 的抑制性突触传递和可塑性。
Nat Commun. 2023 Mar 15;14(1):1436. doi: 10.1038/s41467-023-37137-0.
3
Expression of a Form of Cerebellar Motor Memory Requires Learned Alterations to the Activity of Inhibitory Molecular Layer Interneurons.表达一种小脑运动记忆需要对抑制性分子层中间神经元的活动进行学习性改变。
J Neurosci. 2023 Jan 25;43(4):601-612. doi: 10.1523/JNEUROSCI.0731-22.2022. Epub 2022 Dec 9.
4
Spatial regulation of coordinated excitatory and inhibitory synaptic plasticity at dendritic synapses.树突突触中协调的兴奋性和抑制性突触可塑性的空间调节。
Cell Rep. 2022 Feb 8;38(6):110347. doi: 10.1016/j.celrep.2022.110347.
5
Advances in the Pathogenesis of Auto-antibody-Induced Cerebellar Synaptopathies.自身抗体诱导性小脑突触病发病机制的研究进展。
Cerebellum. 2023 Feb;22(1):129-147. doi: 10.1007/s12311-021-01359-z. Epub 2022 Jan 22.
6
Cerebellar long-term depression and auto-immune target of auto-antibodies: the concept of LTDpathies.小脑长期抑郁与自身抗体的自身免疫靶点：长期抑郁病的概念
Mol Biomed. 2021 Jan 10;2(1):2. doi: 10.1186/s43556-020-00024-x.
7
Regulation of GABA Receptors Induced by the Activation of L-Type Voltage-Gated Calcium Channels.L型电压门控钙通道激活诱导的GABA受体调节
Membranes (Basel). 2021 Jun 29;11(7):486. doi: 10.3390/membranes11070486.
8
Physiology of Cerebellar Reserve: Redundancy and Plasticity of a Modular Machine.小脑储备的生理学：模块化机器的冗余性与可塑性
Int J Mol Sci. 2021 Apr 30;22(9):4777. doi: 10.3390/ijms22094777.
9
γ2 GABAR Trafficking and the Consequences of Human Genetic Variation.γ2 型γ-氨基丁酸受体转运与人类基因变异的后果
Front Cell Neurosci. 2018 Aug 23;12:265. doi: 10.3389/fncel.2018.00265. eCollection 2018.
10
Graded Control of Climbing-Fiber-Mediated Plasticity and Learning by Inhibition in the Cerebellum.小脑内抑制性调控 climbing-fiber 介导的可塑性和学习。
Neuron. 2018 Sep 5;99(5):999-1015.e6. doi: 10.1016/j.neuron.2018.07.024. Epub 2018 Aug 16.
本文引用的文献
1
Activation of Ca(2+)/calmodulin-dependent protein kinase II in cerebellar granule cells by N-methyl-d-aspartate receptor activation.N-甲基-D-天冬氨酸受体激活引起小脑颗粒细胞中 Ca(2+)/钙调蛋白依赖性蛋白激酶 II 的激活。
Mol Cell Neurosci. 1990 Oct;1(2):133-8. doi: 10.1016/1044-7431(90)90017-x.
2
A synaptic model of memory: long-term potentiation in the hippocampus.记忆的突触模型：海马体中的长时程增强效应
Nature. 1993 Jan 7;361(6407):31-9. doi: 10.1038/361031a0.
3
Long-term depression of IPSPs in rat deep cerebellar nuclei.大鼠小脑深部核团中抑制性突触后电位的长期抑制
Neuroreport. 1993 Jun;4(6):719-22. doi: 10.1097/00001756-199306000-00030.
4
Ca2+/calmodulin-dependent protein kinase II and protein kinase C phosphorylate a synthetic peptide corresponding to a sequence that is specific for the gamma 2L subunit of the GABAA receptor.钙/钙调蛋白依赖性蛋白激酶II和蛋白激酶C使一种合成肽发生磷酸化，该合成肽对应于GABAA受体γ2L亚基特有的一个序列。
J Neurochem. 1993 Jul;61(1):375-7. doi: 10.1111/j.1471-4159.1993.tb03582.x.
5
Phosphorylation and regulation of glutamate receptors by calcium/calmodulin-dependent protein kinase II.钙/钙调蛋白依赖性蛋白激酶II对谷氨酸受体的磷酸化作用及调控
Nature. 1993 Apr 15;362(6421):640-2. doi: 10.1038/362640a0.
6
Long-term potentiation is associated with an increased activity of Ca2+/calmodulin-dependent protein kinase II.长时程增强作用与钙/钙调蛋白依赖性蛋白激酶II的活性增加有关。
J Biol Chem. 1993 Apr 15;268(11):7863-7.
7
Regulation of GABAA receptor function by protein kinase C phosphorylation.蛋白激酶C磷酸化对GABAA受体功能的调节
Neuron. 1994 May;12(5):1081-95. doi: 10.1016/0896-6273(94)90316-6.
8
Long-term synaptic depression in the mammalian brain.哺乳动物大脑中的长期突触抑制
Neuron. 1994 Mar;12(3):457-72. doi: 10.1016/0896-6273(94)90205-4.
9
Long-term modification of inhibitory synaptic transmission in developing visual cortex.发育中的视觉皮层中抑制性突触传递的长期改变。
Neuroreport. 1993 Jul;4(7):907-10. doi: 10.1097/00001756-199307000-00017.
10
Lasting potentiation of inhibition is associated with an increased number of gamma-aminobutyric acid type A receptors activated during miniature inhibitory postsynaptic currents.抑制的持久增强与微小抑制性突触后电流期间激活的A型γ-氨基丁酸受体数量增加有关。
Proc Natl Acad Sci U S A. 1994 Aug 2;91(16):7698-702. doi: 10.1073/pnas.91.16.7698.
Zotero 插件