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躁郁症家族细胞系中的β-肾上腺素能受体结合缺陷。

Beta-adrenoceptor binding defects in cell lines from families with manic-depressive disorder.

作者信息

Wright A F, Crichton D N, Loudon J B, Morten J E, Steel C M

出版信息

Ann Hum Genet. 1984 Jul;48(3):201-14. doi: 10.1111/j.1469-1809.1984.tb01016.x.

Abstract

Binding of 125I-iodohydroxybenzylpindolol to beta-adrenoceptors has been examined in lymphoblastoid cell lines from members of 5 families affected by manic-depressive disorder. Cell lines from 6 manic-depressives, 7 unaffected relatives and 11 non-psychiatric controls were examined. Binding was reduced to less than half of control values in cell lines from 4 out of 6 manic-depressives and only 1 out of 18 unaffected relatives or controls. All the cell lines with reduced beta-adrenoceptor binding came from 3 families; members of the remaining 2 families showed normal binding. These findings suggest that genetic heterogeneity is present in manic-depressive disorder and that a beta-adrenoceptor defect may influence genetic susceptibility to the disorder.

摘要

在来自5个受躁郁症影响家庭的成员的淋巴母细胞系中,研究了125I-碘羟基苄基吲哚洛尔与β-肾上腺素能受体的结合情况。检测了来自6名躁郁症患者、7名未患病亲属和11名非精神疾病对照者的细胞系。6名躁郁症患者中的4名以及18名未患病亲属或对照者中的仅1名的细胞系中,结合减少至对照值的一半以下。所有β-肾上腺素能受体结合减少的细胞系均来自3个家庭;其余2个家庭的成员显示结合正常。这些发现表明躁郁症存在遗传异质性,且β-肾上腺素能受体缺陷可能影响该疾病的遗传易感性。

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