108179-91-5
108179-91-5 结构式
基本信息
8-溴-3-甲基-5-苯基-2,3,4,5-四氢-1H-苯并[D]吖庚因-7-醇氢溴酸盐
CS-2574
SKF83566HG
8-bromo-3-methyl-5-phenyl-1,2,4,5-tetrahydro-3-benzazepin-7-ol:hydrobromide
8-Bromo-3-methyl-5-phenyl-2,3,4,5-tetrahydro-1H-benzo[d]azepin-7-ol hydrobromide
1H-3-Benzazepin-7-ol,8-broMo-2,3,4,5-tetrahydro-3-Methyl-5-phenyl-,hydrobroMide(1
1H-3-Benzazepin-7-ol,8-broMo-2,3,4,5-tetrahydro-3-Methyl-5-phenyl-,hydrobroMide(1:1)
常见问题列表
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D 1 Receptor
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D 5 Receptor
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5-HT 2 Receptor 11 nM (Ki) |
SKF-83566 (0.1 μM-10 μM) causes a concentration-dependent increase in peak evoked extracellular DA concentration ([DA] o ) evoked by single-pulse stimulation, with a maximum 65% increase in peak evoked [DA] o with 5 μM. The EC 50 value of this effect of SKF-83566 is 1.3 μM.SKF-83566 inhibited [ 3 H]DA uptake with an IC 50 of 5.73 μM. Moreover, SKF-83566 more potently inhibits the binding of [ 3 H]CFT, a cocaine analog, with an IC 50 of 0.51 μM in [ 3 H]DA uptake and [ 3 H]CFT binding studies.Similarly, in LLc-PK-rDAT cell, SKF-83566 also inhibits [ 3 H]CFT binding with an IC 50 of 0.77 μM in LLc-PK-rDAT cell membrane preparations.
SKF 83566 hydrobromide (oral administration; 20 µg/mL; 7 days) alone has no effects on altering LTP (115%). However, combinnation of SKF 83566 and nicotine significantly blocks the enhancement of long-term synaptic potentiation (LTP) induced by pretreatment with nicotine (SKF 83566+nicotine+cocaine, 120%; nicotine+cocaine, 143%).
| Animal Model: | Male C57BL6/J mice (6- to 9-wk-old) |
| Dosage: | 20 µg/mL (Together with nicotine for 7 d, followed by the injection of cocaine) |
| Administration: | Oral administration; 7 days |
| Result: | Blocked nicotine and cocaine-induced facilitation of LTP. |