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抑郁症患者血小板纯化质膜上3H-对氨基可乐定结合增加。

Elevated 3H-para-aminoclonidine binding to platelet purified plasma membranes from depressed patients.

作者信息

Piletz J E, Halaris A, Saran A, Marler M

机构信息

Department of Psychiatry, Case Western Reserve University, Cleveland, Ohio.

出版信息

Neuropsychopharmacology. 1990 Jun;3(3):201-10.

PMID:1973039
Abstract

Purified platelet plasma membranes were used to compare 3H-para-aminoclonidine binding in 18 depressed patients and 24 sex- and age-matched, healthy control subjects. Two site-selective concentrations of the radioligand were used (0.06 and 1.5 nmol/L) to investigate two high-affinity 3H-para-aminoclonidine binding sites. Radioligand binding was significantly elevated in platelets of depressed patients at both concentrations of 3H-para-aminoclonidine whether expressed per milligram protein, per platelet, or per square micrometer of platelet surface area (each p less than 0.02). These data agree with most previous studies, suggesting that a subset of platelet alpha 2 adrenoceptors, recognized by clonidine and its derivative para-aminoclonidine, is upregulated in depressed patients. By using purified plasma membranes, our data rule out the possibility that an inhibitor may have masked receptor binding in previous studies which used total platelet lysates. The present findings thus support the alpha 2 adrenoceptor hypersensitivity theory of depression.

摘要

纯化的血小板质膜被用于比较18例抑郁症患者与24例性别和年龄匹配的健康对照者的3H-对氨基可乐定结合情况。使用两种位点选择性浓度的放射性配体(0.06和1.5 nmol/L)来研究两个高亲和力的3H-对氨基可乐定结合位点。无论以每毫克蛋白质、每个血小板还是每平方微米血小板表面积来表示,在两种浓度的3H-对氨基可乐定条件下,抑郁症患者血小板中的放射性配体结合均显著升高(每个p值均小于0.02)。这些数据与大多数先前的研究一致,表明可乐定及其衍生物对氨基可乐定所识别的血小板α2肾上腺素能受体的一个亚群在抑郁症患者中上调。通过使用纯化的质膜,我们的数据排除了在先前使用全血小板裂解物的研究中抑制剂可能掩盖受体结合的可能性。因此,目前的研究结果支持抑郁症的α2肾上腺素能受体超敏理论。

相似文献

1
Elevated 3H-para-aminoclonidine binding to platelet purified plasma membranes from depressed patients.抑郁症患者血小板纯化质膜上3H-对氨基可乐定结合增加。
Neuropsychopharmacology. 1990 Jun;3(3):201-10.
2
Super high affinity 3H-para-aminoclonidine binding to platelet adrenoceptors in depression.超高度亲和性的3H-对氨基可乐定与抑郁症患者血小板肾上腺素能受体的结合
Prog Neuropsychopharmacol Biol Psychiatry. 1988;12(4):541-53. doi: 10.1016/0278-5846(88)90113-3.
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Desipramine lowers tritiated para-aminoclonidine binding in platelets of depressed patients.去甲丙咪嗪降低抑郁症患者血小板中氚标记对氨基可乐定的结合力。
Arch Gen Psychiatry. 1991 Sep;48(9):813-20. doi: 10.1001/archpsyc.1991.01810330037006.
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Binding of [3H]-p-aminoclonidine to alpha 2-adrenoceptor states plus a non-adrenergic site on human platelet plasma membranes.[3H]-对氨基可乐定与人血小板质膜上α2-肾上腺素能受体状态及一个非肾上腺素能位点的结合。
Biochem Pharmacol. 1991 Jul 15;42(3):569-84. doi: 10.1016/0006-2952(91)90320-5.
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Comparison of 3H-para-aminoclonidine binding to different platelet preparations.3H-对氨基可乐定与不同血小板制剂结合的比较。
J Neural Transm Gen Sect. 1990;82(1):11-29. doi: 10.1007/BF01244831.
6
Sodium inhibits both adenylate cyclase and high-affinity 3H-labeled p-aminoclonidine binding to alpha 2-adrenergic receptors in purified human platelet membranes.钠可抑制纯化的人血小板膜中的腺苷酸环化酶以及高亲和力的3H标记的对氨基可乐定与α2 - 肾上腺素能受体的结合。
Mol Pharmacol. 1982 May;21(3):600-8.
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Relationship between membrane fluidity and adrenoceptor binding in depression.
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Platelet alpha 2-adrenergic receptors in depressed patients and healthy volunteers: the effects of desipramine.
Pharmacopsychiatry. 1992 Jul;25(4):199-206. doi: 10.1055/s-2007-1014406.
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p-[125I]iodoclonidine is a partial agonist at the alpha 2-adrenergic receptor.对-[¹²⁵I]碘可乐定是α₂肾上腺素能受体的部分激动剂。
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Platelet I1-imidazoline binding sites are elevated in depression but not generalized anxiety disorder.血小板I1-咪唑啉结合位点在抑郁症中升高,但在广泛性焦虑症中未升高。
J Psychiatr Res. 1996 May-Jun;30(3):147-68. doi: 10.1016/0022-3956(96)00005-2.

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Chronic treatment with the monoamine oxidase inhibitors clorgyline and pargyline down-regulates non-adrenoceptor [3H]-idazoxan binding sites in the rat brain.
用单胺氧化酶抑制剂氯吉兰和帕吉林进行长期治疗可下调大鼠脑中的非肾上腺素能受体[3H] - 咪唑克生结合位点。
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The effects of phenelzine and other monoamine oxidase inhibitor antidepressants on brain and liver I2 imidazoline-preferring receptors.苯乙肼及其他单胺氧化酶抑制剂抗抑郁药对脑和肝脏I2咪唑啉优先受体的影响。
Br J Pharmacol. 1995 Feb;114(4):837-45. doi: 10.1111/j.1476-5381.1995.tb13280.x.
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J Neural Transm Gen Sect. 1990;82(1):11-29. doi: 10.1007/BF01244831.