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[Effects of free radicals and amyloid beta protein on the currents of expressed rat receptors in Xenopus oocytes].

作者信息

Huang F N, Zhang B L, Li W B, Cui X, Han Z T, Fang Z Y

机构信息

Department of Neurobiology, Institute of Gerontology and Geriatrics, Chinese PLA General Hospital and Postgraduate Medical School, Beijing 100853, China.

出版信息

Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2001 May;17(2):109-12.

Abstract

AIM

To investigate the effects of free radicals (FRs) and amyloid beta protein (A beta 1-40) on the functions of expressed neurotransmitter receptors (NRs) from rat brains in Xenopus oocytes.

METHODS

Total RNA and Messenger RNA (mRNA) was prepared from 3-month-old Wistar rat brain tissues with Promega kits and microinjected into mature Xenopus oocytes (stage V - VI) with 50 nl (50 ng) for each oocyte for receptor expression and their currents were recorded with double electrode voltage clamp technique. Superoxide anion free radicals (SAFRs) and A beta 1-40 was added 12 h, 24 h, 96 h to incubation solution before recording.

RESULTS

The results showed that oocytes expressed mACh, glutamate, dopamine, serotonin and gamma-aminobutyric acid receptors. The current characteristics of these receptors were inward currents carried by chloride ion with their equilibrium potentials close to - 22 mV. A beta 1-40 and free radicals had a kind of inhibitory effect on the expressed GluR. When treated with 60 nmol/L A beta 1-40 over 24 h, the currents of GluR significantly decreased (25% off, P < :0.01). When oocytes were co-treated with 60 nmol/L A beta 1-40 and SAFRs over a period of 12 h, the currents of glutamate receptor significantly decreased (21% of P < 0.05), and the decreased percentage reached 52% over 24h co-treated with 60 nmol/L A beta 1-40 and SAFRs. Vitamin E had partial antagonistic effect against these effects.

CONCLUSION

The result suggests that A beta has a kind of inhibitory effects upon glutamate receptor, which is similar to those of free radicals. Their effects can be antagonized by vitamin E. This implies that A beta may play roles via inhibiting receptor function in pathophysiology of Alzheimer's disease.

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