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1 ine (1 mM), or a combination of dopamine and nomifensine.
2 increase in [(3)H]-DA release was blocked by nomifensine.
3 determined before and after the injection of nomifensine.
4 e rats was infused with dopamine (1 microM), nomifensine (1 mM), or a combination of dopamine and nom
5 with two other blockers of dopamine uptake, nomifensine (10 mg/kg, i.p.) and 3beta-(p-chlorophenyl)t
6 tection of dopaminergic nerve terminals with nomifensine abolished MPTP-mediated phosphorylation and
7 ection with the dopamine reuptake inhibitor, nomifensine, abolished striatal dopaminergic neurotoxici
8 d that, similar to cocaine, the DAT blockers nomifensine and bupropion were less effective at inhibit
9 tion were used to investigate the effects of nomifensine and ethanol (EtOH) on exogenous norepinephri
12 xy-3beta-(4-flourophenyl)tropane (beta-CFT), nomifensine, benztropine, or (-)-cocaine, 100- to 1000-f
14 ent infusions of the D1 and D2 blockers with nomifensine brought sucrose ingestion back near to contr
16 dopamine signals indicated that cocaine and nomifensine increased the K(m) for dopamine uptake where
18 e dopamine recovery, and (2) estradiol, like nomifensine, increases the recovery of exogenously appli
20 riment 2 responses to the DA uptake blocker, nomifensine (NMF), were assessed in these preparations.
22 and they also demonstrate that the effect of nomifensine on exogenous NE clearance in vivo in the cer
24 t effects of the dopamine reuptake inhibitor nomifensine on recorded single-vesicle release events fr
27 prevented nigral degeneration (deprenyl and nomifensine pretreatment) also prevented the degeneratio
28 The dopamine transporter (DAT) inhibitor, nomifensine, similarly inhibited basal and amphetamine-i
29 rogen and similarities to that obtained with nomifensine suggest that estrogen may be inhibiting dopa
30 tion of 7.7 min showed that the injection of nomifensine transiently increased dopamine and 3-methoxy
31 intraperitoneal) of the DA uptake inhibitor, nomifensine, was significantly less efficacious in augme
32 H23390, sulpiride) and the DA uptake blocker nomifensine were introduced into NAcc while measuring bo
33 T inhibitors, such as cocaine, mazindol, and nomifensine, when administered with AMPH, blocked the re
34 uoxetine, cocaine, nisoxetine, mazindol, and nomifensine, whereas recognition of substrates, includin
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