Morelli M, Carboni E, Cozzolino A, Tanda G L, Pinna A, Di Chiara G
Department of Toxicology, University of Cagliari, Italy.
J Neurochem. 1992 Sep;59(3):1158-60. doi: 10.1111/j.1471-4159.1992.tb08359.x.
Extracellular dopamine (DA) concentrations estimated by transcerebral dialysis and D1-dependent c-fos expression, as demonstrated by Fos immunohistochemistry, were studied after blockade of DA reuptake by GBR-12909. Rats implanted with dialysis probes in the dorsal caudate-putamen did not show any Fos-positive neuronal labeling in the implanted area or in the rest of the caudate-putamen. Administration of GBR-12909 dose-dependently increased DA output in dialysates and resulted in the appearance in the caudate-putamen of Fos-positive neurons whose density was related to the dose of GBR-12909 and to the increase in extracellular concentrations of DA. The D1 antagonist SCH-23390 blocked GBR-12909-induced activation of Fos while potentiating the stimulation of DA output. The results show that following blockade of DA reuptake by GBR-12909, the induction of Fos is related to stimulation of D1 receptors by extracellular DA. Combination of brain dialysis with Fos immunohistochemistry might provide a method for estimating the functional significance of extracellular DA as measured by brain microdialysis.
通过脑透析估计的细胞外多巴胺（DA）浓度以及通过Fos免疫组织化学证实的D1依赖性c-fos表达，在使用GBR-12909阻断DA再摄取后进行了研究。在背侧尾状核-壳核植入透析探针的大鼠，在植入区域或尾状核-壳核的其余部分未显示任何Fos阳性神经元标记。给予GBR-12909剂量依赖性地增加了透析液中的DA输出，并导致尾状核-壳核中出现Fos阳性神经元，其密度与GBR-12909的剂量以及细胞外DA浓度的增加有关。D1拮抗剂SCH-23390阻断了GBR-12909诱导的Fos激活，同时增强了对DA输出的刺激。结果表明，在使用GBR-12909阻断DA再摄取后，Fos的诱导与细胞外DA对D1受体的刺激有关。脑透析与Fos免疫组织化学的结合可能提供一种方法，用于评估通过脑微透析测量的细胞外DA的功能意义。
