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本文引用的文献

1
Multiple Ca2+ channel types coexist to regulate synaptosomal neurotransmitter release.多种钙离子通道类型共同存在以调节突触体神经递质释放。
Proc Natl Acad Sci U S A. 1993 Oct 15;90(20):9518-22. doi: 10.1073/pnas.90.20.9518.
2
The glycine site of the NMDA receptor--five years on.NMDA受体的甘氨酸位点——五年之后
Trends Pharmacol Sci. 1993 Jan;14(1):20-5. doi: 10.1016/0165-6147(93)90108-v.
3
A toxin fraction (FTX) from the funnel-web spider poison inhibits dihydropyridine-insensitive Ca2+ channels coupled to catecholamine release in bovine adrenal chromaffin cells.漏斗网蜘蛛毒液中的一种毒素组分（FTX）可抑制牛肾上腺嗜铬细胞中与儿茶酚胺释放相关的二氢吡啶不敏感型Ca2+通道。
J Neurochem. 1993 Mar;60(3):908-13. doi: 10.1111/j.1471-4159.1993.tb03236.x.
4
Effects of stimulus intensity on the inhibition by omega-conotoxin GVIA and neomycin of K(+_-evoked [3H]norepinephrine release from hippocampal brain slices and synaptosomal calcium influx.刺激强度对ω-芋螺毒素GVIA和新霉素抑制海马脑片K⁺诱发的[³H]去甲肾上腺素释放及突触体钙内流的影响。
Biochem Pharmacol. 1993 Jan 7;45(1):165-71. doi: 10.1016/0006-2952(93)90389-e.
5
Energy-dependent accumulation of neuron blockers causes selective inhibition of neurotransmitter uptake by brain synaptic vesicles.神经元阻滞剂的能量依赖性积累导致脑突触小泡对神经递质摄取的选择性抑制。
Arch Biochem Biophys. 1993 Sep;305(2):278-81. doi: 10.1006/abbi.1993.1423.
6
Analysis of rapid calcium signals in synaptosomes.突触体中快速钙信号的分析。
Neurochem Int. 1993 Oct;23(4):331-41. doi: 10.1016/0197-0186(93)90077-i.
7
Excitatory amino acid action on the release of brain neurotransmitters and neuromodulators: biochemical studies.兴奋性氨基酸对脑神经递质和神经调质释放的作用：生化研究
Prog Neurobiol. 1993 Feb;40(2):223-47. doi: 10.1016/0301-0082(93)90023-l.
8
Metabotropic glutamate receptors in brain function and pathology.代谢型谷氨酸受体在脑功能与病理学中的作用
Trends Pharmacol Sci. 1993 Jan;14(1):13-20. doi: 10.1016/0165-6147(93)90107-u.
9
Initial release of [3H]dopamine from rat striatal synaptosomes: correlation with calcium entry.大鼠纹状体突触体中[3H]多巴胺的初始释放：与钙内流的相关性。
J Neurosci. 1983 Apr;3(4):703-13. doi: 10.1523/JNEUROSCI.03-04-00703.1983.
10
A venom peptide with a novel presynaptic blocking action.一种具有新型突触前阻断作用的毒液肽。
Nature. 1984;308(5956):282-4. doi: 10.1038/308282a0.

海马体中突触前谷氨酸受体对多巴胺和去甲肾上腺素释放以及细胞内钙离子浓度的调节作用

Modulation of dopamine and noradrenaline release and of intracellular Ca2+ concentration by presynaptic glutamate receptors in hippocampus.

作者信息

Malva J O, Carvalho A P, Carvalho C M

机构信息

Department of Zoology, University of Coimbra, Portugal.

出版信息

Br J Pharmacol. 1994 Dec;113(4):1439-47. doi: 10.1111/j.1476-5381.1994.tb17158.x.

DOI:10.1111/j.1476-5381.1994.tb17158.x
PMID:7534187
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1510498/
Abstract
  1. We studied the release of [3H]-dopamine and [3H]-noradrenaline (NA) from hippocampal synaptosomes induced by glutamate receptors and the associated Ca2+ influx through Ca2+ channels. The release of tritiated neurotransmitters was studied by use of superfusion system and the intracellular free Ca2+ concentration ([Ca2+]i) was determined by a fluorimetric assay with Indo-1 as a probe for Ca2+. 2. Presynaptic glutamate receptor activation induced Ca(2+)-dependent release of [3H]-dopamine and [3H]-NA from rat hippocampal synaptosomes. Thus, L-glutamate induced the release of both neurotransmitters in a dose-dependent manner (EC50 = 5.62 microM), and the effect of 100 microM L-glutamate was inhibited by 83.8% in the presence of 10 microM 6-cyano-7-nitroquinoxaline-2,3-dioxine (CNQX), but was not affected by 1 microM (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]-cyclohepten-5,10-imine (MK-801). 3. Other glutamate receptor agonists also stimulated the Ca(2+)-dependent release of [3H]-dopamine and [3H]-NA as follows: N-methyl-D-aspartate (NMDA), at 200 microM, released 3.65 +/- 0.23% of the total 3H catecholamines, and this effect was inhibited by 81.2% in the presence of 1 microM MK-801; quisqualate (50 microM), S-alpha-amino-3-hydroxy-5-methyl-4-isoxazolopropionic acid (AMPA) (100 microM) or kainate (100 microM) released 1.57 +/- 0.26%, 1.93 +/- 0.17% and 2.09 +/- 0.22%, of the total 3H catecholamines, respectively. 4. The ionotropic glutamate receptor agonist, AMPA, induced an increase in the [Ca2+]i which was inhibited by 58.6% in the presence of 10 microM CNQX. In contrast, the increase in [Ca2+]i due to stimulation by glutamate was not sensitive to CNQX or MK-801.5. Nitrendipine, at I JAM, did not inhibit the neurotransmitter release induced by AMPA, but, both 0.5 micro M -conotoxin GVIA (w-CgTx) and 100 nM w-Aga IVA reduced catecholamine release to 49.03 +/- 3.79% and 46.06 +/- 10.51% of the control, respectively. In the presence of both toxins the release was reduced to 12.58 +/- 4.64% of the control.6. The results indicate that activation of presynaptic glutamate receptors of the NMDA and non-NMDA type induces the release of [3H]-dopamine and [H]-NA from rat hippocampal synaptosomes and that the release induced by AMPA involves the activation of N- and P-type Ca2" channels which allow the influx of Ca2" that triggers the 3H catecholamines release.
摘要
  1. 我们研究了谷氨酸受体诱导的[3H]-多巴胺和[3H]-去甲肾上腺素（NA）从海马突触体的释放以及通过钙通道伴随的Ca2+内流。使用灌流系统研究了氚标记神经递质的释放，并通过以Indo-1作为Ca2+探针的荧光测定法测定细胞内游离Ca2+浓度（[Ca2+]i）。2. 突触前谷氨酸受体激活诱导大鼠海马突触体中[3H]-多巴胺和[3H]-NA的Ca(2+)依赖性释放。因此，L-谷氨酸以剂量依赖性方式诱导两种神经递质的释放（EC50 = 5.62 microM），在10 microM 6-氰基-7-硝基喹喔啉-2,3-二酮（CNQX）存在下，100 microM L-谷氨酸的作用被抑制83.8%，但不受1 microM（+）-5-甲基-10,11-二氢-5H-二苯并[a,d]-环庚烯-5,10-亚胺（MK-801）影响。3. 其他谷氨酸受体激动剂也如下刺激[3H]-多巴胺和[3H]-NA的Ca(2+)依赖性释放：200 microM的N-甲基-D-天冬氨酸（NMDA）释放了总3H儿茶酚胺的3.65 +/- 0.23%，在1 microM MK-801存在下，这种作用被抑制81.2%；50 microM的quisqualate、100 microM的S-α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）或100 microM的海人藻酸分别释放了总3H儿茶酚胺的1.57 +/- 0.26%、1.93 +/- 0.17%和2.09 +/- 0.22%。4. 离子型谷氨酸受体激动剂AMPA诱导[Ca2+]i增加，在10 microM CNQX存在下被抑制58.6%。相反，谷氨酸刺激引起的[Ca2+]i增加对CNQX或MK-801不敏感。5. 1 microM的尼群地平不抑制AMPA诱导的神经递质释放，但0.5 microM的ω-芋螺毒素GVIA（ω-CgTx）和100 nM的ω-银环蛇毒素IVA分别将儿茶酚胺释放降低至对照的49.03 +/- 3.79%和46.06 +/- 10.51%。在两种毒素存在下，释放降低至对照的12.58 +/- 4.64%。6. 结果表明，NMDA和非NMDA型突触前谷氨酸受体的激活诱导大鼠海马突触体中[3H]-多巴胺和[H]-NA的释放，并且AMPA诱导的释放涉及N型和P型Ca2"通道的激活，这些通道允许Ca2"内流，从而触发3H儿茶酚胺的释放。