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[γ-氨基丁酸与谷氨酸脱羧酶]

[Gamma-aminobutyric acid and glutamate decarboxylase].

作者信息

Turský T

机构信息

Ustav lekárskej chémie, biochémie a klinickej biochémie v Bratislave, Slovakia.

出版信息

Bratisl Lek Listy. 1993 Jul;94(7):366-72.

PMID:8004482
Abstract

Gamma-aminobutyric acid (GABA) is the main inhibitory neurotransmitter in the CNS, taking part in processes which are now relatively well understood but also in processes which are remarkable progress has been achieved. The most thoroughly studied field of GABA operation is its role of inhibitory neurotransmitter realized through the mediation of GABA-A and GABA-B receptors. There are at least 40 per cent of synaptic inhibitory events in the CNS in which the neurotransmitter action of GABA is involved. The action of GABA on GABA-A receptor, a Cl- channel, is influenced by benzodiazepines, barbiturates and other substances, suggesting that some neurological and psychiatric diseases are connected with the function of GABA-A receptor. In addition to synaptic inhibition, GABA has several metabolic regulatory functions. GABA is produced not only in neurons but also in beta cells of the pancreas and in tubular cells of the kidney cortex. Its role in these parenchymatous cells is not sufficiently understood. Similarly as GABA, glutamic acid decarboxylase (GAD), an enzyme catalysing GABA formation from glutamate, has also been intensively studied. GAD structure, its function in various parts of the CNS and in some parenchymatous cells, and the regulation of GAD activity are still in the focus of interest. Recently GAD has been demonstrated to act as autoantigen in the rare neurological disease "stiff man syndrome" (SMS) and in insulin-dependent diabetes mellitus (IDDM). In the presented paper a short review of GABA functions, GAD properties and of the antigenic feature of GAD are given. (Fig. 7, Ref. 41.)

摘要

γ-氨基丁酸(GABA)是中枢神经系统中主要的抑制性神经递质,它参与了目前已相对了解的过程,也参与了已取得显著进展的过程。GABA作用最深入研究的领域是其作为抑制性神经递质,通过GABA-A和GABA-B受体介导所发挥的作用。中枢神经系统中至少40%的突触抑制事件涉及GABA的神经递质作用。GABA对作为氯离子通道的GABA-A受体的作用受苯二氮䓬类、巴比妥类及其他物质影响,这表明一些神经和精神疾病与GABA-A受体的功能有关。除突触抑制外,GABA还有多种代谢调节功能。GABA不仅在神经元中产生,也在胰腺的β细胞和肾皮质的肾小管细胞中产生。其在这些实质细胞中的作用尚未得到充分了解。与GABA类似,谷氨酸脱羧酶(GAD),一种催化由谷氨酸形成GABA的酶,也受到了深入研究。GAD的结构、其在中枢神经系统各部位及一些实质细胞中的功能,以及GAD活性的调节仍备受关注。最近已证明GAD在罕见的神经疾病“僵人综合征”(SMS)和胰岛素依赖型糖尿病(IDDM)中作为自身抗原起作用。本文对GABA的功能、GAD的特性以及GAD的抗原特性进行了简要综述。(图7,参考文献41。)

相似文献

1
[Gamma-aminobutyric acid and glutamate decarboxylase].[γ-氨基丁酸与谷氨酸脱羧酶]
Bratisl Lek Listy. 1993 Jul;94(7):366-72.
2
Inhibition of gamma-aminobutyric acid synthesis by glutamic acid decarboxylase autoantibodies in stiff-man syndrome.僵人综合征中谷氨酸脱羧酶自身抗体对γ-氨基丁酸合成的抑制作用。
Ann Neurol. 1998 Aug;44(2):194-201. doi: 10.1002/ana.410440209.
3
Autoimmunity to glutamic acid decarboxylase (GAD) in Stiff-Man syndrome and insulin-dependent diabetes mellitus.僵人综合征和胰岛素依赖型糖尿病中针对谷氨酸脱羧酶(GAD)的自身免疫反应。
Trends Neurosci. 1991 Oct;14(10):452-7. doi: 10.1016/0166-2236(91)90044-u.
4
Identification of a dominant epitope of glutamic acid decarboxylase (GAD-65) recognized by autoantibodies in stiff-man syndrome.僵人综合征中自身抗体识别的谷氨酸脱羧酶(GAD - 65)主要表位的鉴定。
J Exp Med. 1993 Dec 1;178(6):2097-106. doi: 10.1084/jem.178.6.2097.
5
Autoantibodies to GABA-ergic neurons and pancreatic beta cells in stiff-man syndrome.僵人综合征中针对γ-氨基丁酸能神经元和胰腺β细胞的自身抗体。
N Engl J Med. 1990 May 31;322(22):1555-60. doi: 10.1056/NEJM199005313222202.
6
Synaptic vesicle-associated glutamate decarboxylase: identification and relationship to insulin-dependent diabetes mellitus.突触小泡相关谷氨酸脱羧酶:鉴定及其与胰岛素依赖型糖尿病的关系。
J Neurosci Res. 1995 Jan 1;40(1):134-7. doi: 10.1002/jnr.490400115.
7
GABAergic dysfunction in mGlu7 receptor-deficient mice as reflected by decreased levels of glutamic acid decarboxylase 65 and 67kDa and increased reelin proteins in the hippocampus.代谢型谷氨酸受体7(mGlu7)缺陷小鼠中的γ-氨基丁酸(GABA)能功能障碍,表现为海马中谷氨酸脱羧酶65和67kDa水平降低以及Reelin蛋白增加。
Brain Res. 2010 Jun 2;1334:12-24. doi: 10.1016/j.brainres.2010.03.078. Epub 2010 Mar 29.
8
Identification of the 64K autoantigen in insulin-dependent diabetes as the GABA-synthesizing enzyme glutamic acid decarboxylase.胰岛素依赖型糖尿病中64K自身抗原被鉴定为γ-氨基丁酸合成酶谷氨酸脱羧酶。
Nature. 1990 Sep 13;347(6289):151-6. doi: 10.1038/347151a0.
9
A novel mechanism for GABA synthesis and packaging into synaptic vesicles.一种将γ-氨基丁酸合成并包装到突触小泡中的新机制。
Neurochem Int. 2009 Jul-Aug;55(1-3):9-12. doi: 10.1016/j.neuint.2009.01.020. Epub 2009 Feb 6.
10
Stiff-man syndrome: possible autoimmune etiology targeted against GABA-ergic cells.僵人综合征:可能存在针对γ-氨基丁酸能细胞的自身免疫病因。
Clin Neuropathol. 1997 Jul-Aug;16(4):214-9.