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AVP_(4-8)结合点在大鼠海马内的分布和AVP_(4-8)对其受体发育的影响:放射自显影研究 被引量:4

AUTORADIOGRAPHIC APPROACH TO THE DEVELOPMENTAL STUDY ON THE BINDING SITES OF AVP_(4-8)IN RAT HIPPOCAMPUS
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摘要 本文利用放射自显影方法结合神经毒对海马神经元的选择性损毁观察AVP(4-8)结合点在大鼠海马内的分布和定位;利用外源性AVP(4-8)对新生大鼠的处理,观察海马AVP(4-8)结合点的发育调节。在成年大鼠海马内,AVP(4-8)结合点集中分布在整个海马的锥体细胞层和齿回的颗粒细胞层。秋水仙碱处理后,齿回颗粒细胞层消失,齿回区的AVP(4-8)结合点也消失。红藻氨酸(Kainicacid)处理后海马CA3-CA4的锥体细胞层消失,该区的AVP(4-8)结合点也消失。新生大鼠海马锥体细胞层的AVP(4-8)结合点在出生后第6天开始出现,齿回颗粒细胞层的AVP(4-8)结合点在出生后第7天开始出现。然而,新生大鼠每天经外源性AVP(4-8)处理,海马锥体细胞层和齿回颗粒细胞层的结合点均在出生后第5天已变得十分稠密。本文就大鼠海马AVP(4-8)结合点的特异性分布和AVP(4-8)处理促进海马AVP(4-8)结合点的发育与成年后大鼠学习能力的提高的相互关系作了讨论。 The localization of the 35S-labelled AVP4-8 binding sites in the rat hippocampus was studied by using autoradiographic approach via observing the selective damages of hippocampal neurons by neurotoxins, and the developmental regulation of the hippocampal AVP4-8 receptor by pretreatment with exogenous AVP4-8 was observed. In adult rat hippocampus, the binding sites of AVP4-8 were assembled on the whole hippocampal pyramidal cell layer and granular cell layer of the dentate gyrus. Treatment of colchicine caused parallel disappearances of granular cells and the AVP4-8 binding sites in the gyrus, while treatment of kaininc acid destroyed the CA3-CA4 pyramidal cell layer and abolished the binding sites in this area. The developmental emer nces of AVP4-8 binding sites were normally on postnatal day 6 in pyramidal cell layer and postnatul day 7in the dentate gyrus. However, postnatal daily treatments of exogenous AVP4-8 enhanced the formations of both pyramidal and dentate binding sites, as they appeared rather densely on postnatal day 5. The characterized distribution of AVP4-8 binding sites in the rat hippocampus and the relationship between their developmental enhancements and facilitation of learning behaviors in mature rat by neonatal treatment of exogenous AVP4-8 were discussed.
出处 《生理学报》 CSCD 北大核心 1994年第5期435-440,共6页 Acta Physiologica Sinica
关键词 神经毒 精氨酸 血管加压素 海马 受体 binding site AVP_(4-8) rat hippocampus brain development
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参考文献4

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同被引文献16

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