正常血压大鼠脑血流短暂减少对纹状体多巴胺释放的影响。

Effect of transient reduction of cerebral blood flow in normotensive rats on striatal dopamine-release.

作者信息

Läer S, Block F, Huether G, Heim C, Sontag K H

机构信息

Max-Planck-Institut für Experimentelle Medizin, Göttingen, Federal Republic of Germany.

出版信息

J Neural Transm Gen Sect. 1993;92(2-3):203-11. doi: 10.1007/BF01244879.

DOI:10.1007/BF01244879

PMID:7690231

Abstract

Bilateral Clamping of both Carotid Arteries (BCCA) in normotensive rats is known to cause a transient reduction in cerebral blood flow. Using in vivo trans-striatal microdialysis and HPLC/ECD we measured the release of dopamine and DA-metabolites under these oligemic conditions. BCCA caused a substantial stimulation of striatal DA-release (40-fold) and a decrease of the outflow of DA-metabolites. The elevated DA-release returned to baseline levels before the onset of reperfusion. Upon reperfusion, DA-metabolites rose above their initial baseline values. Trans-striatal administration of glutamate-diethylester (GDEE, 10 mM) attenuated the oligemia-induced DA-release. A sudden reduction of blood flow appears to disrupt the compartmentation of dopamine in striatal dopaminergic nerve endings in a similar but more moderate manner as compared to ischemia.

摘要

已知在血压正常的大鼠中双侧颈总动脉夹闭（BCCA）会导致脑血流量短暂减少。我们使用体内经纹状体微透析和高效液相色谱/电化学检测法（HPLC/ECD），在这些低灌注条件下测量多巴胺和多巴胺代谢产物的释放。BCCA引起纹状体多巴胺释放大幅增加（40倍），多巴胺代谢产物流出减少。升高的多巴胺释放在再灌注开始前恢复到基线水平。再灌注时，多巴胺代谢产物升至初始基线值以上。经纹状体给予谷氨酸二乙酯（GDEE，10 mM）可减弱低灌注诱导的多巴胺释放。与缺血相比，血流量突然减少似乎以类似但更温和的方式破坏了纹状体多巴胺能神经末梢中多巴胺的分隔。