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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
10 nsitivity to the dopamine reuptake inhibitor nomifensine, and elevated autoreceptor function.
11                     In the young rats, local nomifensine application prolonged exogenous NE clearance
12                     Reverse microdialysis of nomifensine at a dose that increased accumbens DA levels
13 xy-3beta-(4-flourophenyl)tropane (beta-CFT), nomifensine, benztropine, or (-)-cocaine, 100- to 1000-f
14 uction of astrogliosis; neuroprotection with nomifensine blocked these effects of MPTP.
15 ent infusions of the D1 and D2 blockers with nomifensine brought sucrose ingestion back near to contr
16                 In contrast to the effect of nomifensine, EtOH inhibited NE clearance in both young a
17  dopamine signals indicated that cocaine and nomifensine increased the K(m) for dopamine uptake where
18       Treatment with nomifensine or dopamine/nomifensine increased the recovery of dopamine in the ef
19 ration of the dopamine transporter inhibitor nomifensine increases resting DA to a maximum 207 +/- 16
20 e dopamine recovery, and (2) estradiol, like nomifensine, increases the recovery of exogenously appli
21        Experiments with the uptake inhibitor nomifensine indicated that this was caused by enhanced d
22 riment 2 responses to the DA uptake blocker, nomifensine (NMF), were assessed in these preparations.
23      Administration of amphetamine (AMPH) or nomifensine (NOM), drugs which increase synaptic dopamin
24 and they also demonstrate that the effect of nomifensine on exogenous NE clearance in vivo in the cer
25 istent with this, there was little effect of nomifensine on NE clearance in the aged rats.
26 t effects of the dopamine reuptake inhibitor nomifensine on recorded single-vesicle release events fr
27                           On the other hand, nomifensine only enhanced the dopaminergic signal either
28                               Treatment with nomifensine or dopamine/nomifensine increased the recove
29  prevented nigral degeneration (deprenyl and nomifensine pretreatment) also prevented the degeneratio
30    The dopamine transporter (DAT) inhibitor, nomifensine, similarly inhibited basal and amphetamine-i
31 rogen and similarities to that obtained with nomifensine suggest that estrogen may be inhibiting dopa
32 tion of 7.7 min showed that the injection of nomifensine transiently increased dopamine and 3-methoxy
33 ligands as well as after methamphetamine and nomifensine treatment.
34 intraperitoneal) of the DA uptake inhibitor, nomifensine, was significantly less efficacious in augme
35 H23390, sulpiride) and the DA uptake blocker nomifensine were introduced into NAcc while measuring bo
36 T inhibitors, such as cocaine, mazindol, and nomifensine, when administered with AMPH, blocked the re
37 uoxetine, cocaine, nisoxetine, mazindol, and nomifensine, whereas recognition of substrates, includin