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抑郁症患者和健康对照者单个T淋巴细胞中的胞质游离钙离子浓度。

Cytosolic free [Ca2+] in single T-lymphocytes from depressed patients and healthy controls.

作者信息

Vollmayr B, Aldenhoff J B

机构信息

Central Institute of Mental Health, Mannheim, Germany.

出版信息

Eur Arch Psychiatry Clin Neurosci. 1994;243(5):214-7. doi: 10.1007/BF02191576.

DOI:10.1007/BF02191576
PMID:8172933
Abstract

Human lymphocytes are widely used as peripheral models for central neurones. Alterations in immune function have been reported in depressed patients, e.g. mitogen-induced proliferation is impaired during depression. One possible causative mechanism could be altered [Ca2+]i regulation. Phytohaemagglutinin (PHA)-induced rise of [Ca2+]i has been found to be diminished in lymphocyte suspensions from depressed patients (Ecker et al., this issue). We measured PHA-induced rise of [Ca2+]i in single Fura-2 AM-loaded T11+ lymphocytes of patients with major depression and controls to further analyse [Ca2+]i regulation in depression. The [Ca2+]i of resting lymphocytes was 57 +/- 2 nmol/l (mean +/- SEM). There was no difference in resting [Ca2+]i of resting lymphocytes of patients and controls. PHA evoked an increase of [Ca2+]i an 7 out of 14 cells from control subjects up to 400-500 nmol/l. In contrast, only 4 out of 13 cells from depressed patients showed an increase of [Ca2+]i up to 200 nmol/l. In a small fraction of cells from both groups the [Ca2+]i signal is oscillating. Our preliminary data confirm alteration of [Ca2+]i regulation in lymphocytes of depressed patients.

摘要

人类淋巴细胞被广泛用作中枢神经元的外周模型。已有报道称抑郁症患者存在免疫功能改变,例如在抑郁期间丝裂原诱导的增殖受损。一种可能的致病机制可能是[Ca2+]i调节改变。已发现抑郁症患者淋巴细胞悬液中植物血凝素(PHA)诱导的[Ca2+]i升高减弱(埃克等人,本期)。我们测量了重度抑郁症患者和对照组单个Fura-2 AM负载的T11+淋巴细胞中PHA诱导的[Ca2+]i升高,以进一步分析抑郁症中的[Ca2+]i调节。静息淋巴细胞的[Ca2+]i为57±2 nmol/l(平均值±标准误)。患者和对照组静息淋巴细胞的静息[Ca2+]i没有差异。PHA使14名对照受试者中的7个细胞的[Ca2+]i升高至400 - 500 nmol/l。相比之下,抑郁症患者的13个细胞中只有4个细胞的[Ca2+]i升高至200 nmol/l。在两组的一小部分细胞中,[Ca2+]i信号呈振荡状态。我们的初步数据证实了抑郁症患者淋巴细胞中[Ca2+]i调节的改变。

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