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胰腺中β-内啡肽结合的放射自显影定位

Autoradiographic localization of beta-endorphin binding in the pancreas.

作者信息

Zhang M, Zheng M, Schleicher R L

机构信息

Medical Research Service, Veterans Affairs Medical Center (Atlanta), Decatur, Georgia 30033.

出版信息

Mol Cell Neurosci. 1994 Dec;5(6):684-90. doi: 10.1006/mcne.1994.1082.

DOI:10.1006/mcne.1994.1082
PMID:7704443
Abstract

Autoradiographic localization of 125I-labeled beta-endorphin binding in the rabbit pancreas demonstrated specific binding in the pancreatic islet cells. Binding was inhibited by (1) nonradioactive beta-endorphin, (2) the opioid antagonist naloxone, (3) the mu receptor agonists morphine and [D-Ala2, (Me)Phe4, Gly(ol)5]enkephalin, (4) the delta receptor agonist [D-penicillamine2, D-penicillamine5]-enkephalin, (5) the mu and delta agonist met-enkephalin and (6) the delta and kappa agonist dynorphin. Specific binding was not clearly demonstrable in the acinar portion of the rabbit pancreas. The binding characteristics of 125I-beta-endorphin in the pancreatic islets were comparable with those of mu and delta opioid receptors in the rabbit brain. In the pancreas, beta-endorphin binding appeared to be concentrated in discrete areas in the islets. Combined immunohistochemistry and autoradiography demonstrated that beta-endorphin binding was primarily concentrated in the glucagon-containing alpha and somatostatin-containing delta cells, but was also found in the insulin-containing beta cells to a lesser extent. Given the intraislet location of the opioid binding sites, and our previous finding of immunoreactive beta-endorphin in the pancreatic beta cells and the inhibitory effect of beta-endorphin on insulin secretion, it appears that beta-endorphin may serve a paracrine or autocrine function in the regulation of pancreatic hormone secretion.

摘要

125I标记的β-内啡肽在兔胰腺中的放射自显影定位显示,在胰岛细胞中有特异性结合。结合受到以下物质的抑制:(1)非放射性β-内啡肽;(2)阿片类拮抗剂纳洛酮;(3)μ受体激动剂吗啡和[D-Ala2,(Me)Phe4,Gly(ol)5]脑啡肽;(4)δ受体激动剂[D-青霉胺2,D-青霉胺5]-脑啡肽;(5)μ和δ激动剂甲硫脑啡肽;(6)δ和κ激动剂强啡肽。在兔胰腺的腺泡部分未明确显示出特异性结合。125I-β-内啡肽在胰岛中的结合特性与兔脑中μ和δ阿片受体的结合特性相当。在胰腺中,β-内啡肽结合似乎集中在胰岛的离散区域。免疫组织化学和放射自显影相结合表明,β-内啡肽结合主要集中在含胰高血糖素的α细胞和含生长抑素的δ细胞中,但在含胰岛素的β细胞中也有较少程度的发现。鉴于阿片类结合位点在胰岛内的位置,以及我们之前在胰腺β细胞中发现的免疫反应性β-内啡肽以及β-内啡肽对胰岛素分泌的抑制作用,似乎β-内啡肽可能在胰腺激素分泌的调节中发挥旁分泌或自分泌功能。

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Transcranial electrostimulation activates reparative regeneration and the insulin-producing function of pancreatic B-cells in alloxan diabetes in rats.经颅电刺激可激活大鼠四氧嘧啶糖尿病模型中胰腺β细胞的修复性再生及胰岛素分泌功能。
Neurosci Behav Physiol. 2007 May;37(4):341-7. doi: 10.1007/s11055-007-0019-2.
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Transcranial stimulation normalizes blood sugar levels in alloxan diabetes in rats.
经颅刺激可使大鼠四氧嘧啶糖尿病模型的血糖水平恢复正常。
Neurosci Behav Physiol. 2006 Jan;36(1):35-7. doi: 10.1007/s11055-005-0160-8.