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Hypoxia influences enkephalin release in rats

Chen, Xue‐Qun; Du, Ji‐Zeng

Neurophysiology

To investigate hypoxia effects on leucine‐enkephalin (L‐ENK) levels of median eminence (ME) of hypothalamus in rats, and the possible glucocorticoid involvement in modulation. Hypoxia was stimulated in a hypobaric chamber. L‐ENK levels were measured by specific radioimmunoassay during acute, and a comparison of L‐ENK alteration was taken for bilateral adrenalectomy (ADX) with or without a replacement of dexamethasone (DEX). Acute hypoxia 10.8% O2 for 30 min and 2 h markedly enhanced L‐ENK levels of ME from 23.99 ± 7.25 in control to 51.26 ± 16.96 (P <0.01), 53.29 ± 26.10 ng/mg protein (p <0.01), and acute hypoxia at 8.2% O2 significantly increased L‐ENK of ME to 36.76 ± 15.25 (p <0.05) and 32.09 ± 3.58 ng/mg protein (p <0.05). The increased L‐ENK was returned to normoxic level when hypoxia (10.8% O2) exposure lasted for 24 h. After ADX, 10.8% O2 hypoxia induced a sharp decline of L‐ENK in the ME, but this decline was completely reversed by treatment with DEX (500 μg/rat, i.p.). Acute hypoxia increases L‐ENK level of hypothalamic ME in rats, which may present a reduced and /or inhibited release of L‐ENK, acting through a fast negative feedback mechanism of acute hypoxia activated high circulating glucocorticoid level.

1 Division of Neurobiology and Physiology, College of Life Sciences, Yuquan Campus, Zhejiang University, Hangzhou 310027, PR China

2 Corresponding Author: Ji‐Zeng Du

Acknowledgements: This research is supported by National Science Foundation of China (NSFC), No. 39770288. The authors thank Dr P.S. Timiras, from the Department of Molecular and Cell Biology at the University of California, Berkeley for her valuable review of the manuscript.

Received 28 February 2000; accepted 3 March 2000

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