Nomifensine: a new potent inhibitor of dopamine uptake into synaptosomes from rat brain corpus striatum

Hunt, Peter; Kannengiesser, Marie-Hélène; Raynaud, Jean‐Pierre

doi:10.1111/j.2042-7158.1974.tb09294.x

Cited by 295 publications

(85 citation statements)

References 7 publications

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“…The observation that 5-HT uptake into synaptosomes from rat striatum was partially inhibited (Hunt et al, 1974;Schacht & Heptner, 1974) by the catecholamine uptake inhibitor nomifensine suggests that 5-HT may also be taken up into structures other than 5-hydroxytryptaminergic nerve endings (Kelly et al, 1985). We interpret the observed phenomena as follows: both nomifensine and 6-nitroquipazine inhibited the transport of monoamines selectively into the appropriate neurones, i.e.…”

Section: Discussionmentioning

confidence: 69%

False labelling of dopaminergic terminals in the rabbit caudate nucleus: uptake and release of [³H]‐5‐hydroxytryptamine

Feuerstein

Hertting

Lupp

et al. 1986

British J Pharmacology

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nomifensine (1, 10 gAM) reduced the tritium accumulation to 65% whereas 6-nitroquipazine (1 JM) was ineffective. The combination of both drugs (1 JAM each) led to a further decrease to about 15%.3 The uptake of [3H]-dopamine into hippocampal slices was blocked by both nomifensine (I JM) and 6-nitroquipazine (I ILM) whereas in caudate nucleus slices only nomifensine (1, 1OtM) reduced the accumulation of [3H]-dopamine. The combination of both drugs was not more effective than nomifensine alone. The different effects of both uptake inhibitors in the hippocampus and caudate nucleus suggest a neurone specific rather than a substrate specific mode of action. 4 In caudate nucleus slices incubated with [3H]-5-HT and superfused continuously the electrically evoked 5-HT release was diminished by the D2-dopamine receptor agonist LY 171555 and enhanced by the D2-receptor antagonist domperidone. If, however, the labelling of caudate nucleus slices was performed in the presence of I JAM or 1OJM nomifensine, the modulation of 5-HT release via D2-receptors was reduced or abolished, respectively. In the hippocampus both LY 171555 and domperidone were completely ineffective in modulating 5-HT release regardless of the absence or presence of nomifensine.

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Section: Discussionmentioning

confidence: 69%

False labelling of dopaminergic terminals in the rabbit caudate nucleus: uptake and release of [³H]‐5‐hydroxytryptamine

Feuerstein

Hertting

Lupp

et al. 1986

British J Pharmacology

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“…Each piece was placed in a scintillation vial and 900 ~1 of Ringer's containing 2 mM isobutylmethylxanthine (IBMX) was added to the vial. Following a 5 min incubation, 100 pl of test substance in Ringer's containing the dopamine uptake inhibitor nomifensine (final concentration 30 pm) was added to the incubation medium and the incubation continued for an additional 10 min (Hunt et al, 1974). For dopamine-blocking experiments, haloperidol was added in the 5 min incubation period prior to the application of the test substance.…”

Section: Camp Experimentsmentioning

confidence: 99%

“…7). In subsequent experiments, nomifensine, a dopamine uptake inhibitor (Hunt et al, 1974), was added to the incubation medium and was found to enhance significantly the accumulation of CAMP signal. In the presence of 30 I.LM nomifensine, the GABA antagonists (100 FM) stimulated an approximate 300 pmol cAMP/mg protein increase above control levels (Fig.…”

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confidence: 99%

Factors affecting release of 3H-dopamine from perfused carp retina

OʼConnor¹,

Dorison²,

Watling³

et al. 1986

J. Neurosci.

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The effects of putative retinal neurotransmitters and several neuropeptides on 3H-dopamine release from isolated perfused carp (Cypriuus curpio) retinas were studied. Of the transmitter candidates tested, only serotonin (S-HT) and the 5-HT agonist tryptamine released "H-dopamine. However, the release evoked by these agents was calcium (Ca*+) independent and not blockable by the 5-HT antagonist methysergide. We also investigated the antagonism of inhibitory inputs as a potential regulatory mechanism for dopamine release and found that the GABA antagonists, bicuculline and picrotoxin, stimulated a dose-dependent release of 3Hdopamine. The effects of the GABA antagonists were dependent on extracellular Ca*+ and could be inhibited by perfusion of the retina with GABA. Bicuculline and picrotoxin also stimulated an increase in CAMP accumulation, which was inhibited by the dopamine antagonist haloperidol. Our results support the hypothesis that the dopaminergic interplexiform cells of the teleost retina are under GABAergic inhibitory control.

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“…Nomifensine, an effective blocker of dopamine uptake (Hunt, Kannengiesser & Raynaud, 1974), produced at the higher dose level (20 mg/kg) an increase in both homovanillic acid (Gerhards, Carenzi & Costa, 1974 and Table 3) and p-tyramine (Table 3). These results are surprising because they are at variance with those obtained after other treatments that increase dopamine turnover (see review by Juorio, 1982a).…”

Section: Discussionmentioning

confidence: 99%

The Effects of Amfonelic Acid and Some Other Central Stimulants on Mouse Striatal Tyramine, Dopamine and Homovanillic Acid

Juorio¹

1982

British J Pharmacology

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1 The concentrations of p-and m-tyramine, dopamine and homovanillic acid were measured in the mouse striatum following the subcutaneous administration of amfonelic acid, (+)-amphetamine or nomifensine.2 The administration of 2.5-25 mg/kg of amfonelic acid produced a reduction in p-tyramine that lasted at least 8 h. m-Tyramine was significantly increased and this was observed between 2 and 24 h after drug treatment. The levels of homovanillic acid were increased within 4 h after amfonelic acid administration.3 (+)-Amphetamine treatment (5 mg/kg) produced a reduction in p-tyramine observed up to 4 h after its administration and no significant changes in m-tyramine. 4 The administration of 10 mg/kg of nomifensine produced no significant changes in p-tyramine, m-tyramine or homovanillic acid. By increasing the dose to 20 mg/kg, nomifensine produced an increase in p-tyramine and homovanillic acid. 5 The present results support the view that amfonelic acid and (+)-amphetamine would respectively release granular or newly synthesized dopamine, both actions being accompanied by an increase in tyrosine hydroxylase activity and dopamine turnover which in turn reduces p-tyramine but produces no change or an increase in m-tyramine.6 The effects of nomifensine were observed after the administration of a relatively high dose (20 mg/kg), that was lethal to some mice (about 20%, at 2 h), and more likely to possess unspecific actions.

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Nomifensine: a new potent inhibitor of dopamine uptake into synaptosomes from rat brain corpus striatum

Cited by 295 publications

References 7 publications

False labelling of dopaminergic terminals in the rabbit caudate nucleus: uptake and release of [³H]‐5‐hydroxytryptamine

False labelling of dopaminergic terminals in the rabbit caudate nucleus: uptake and release of [³H]‐5‐hydroxytryptamine

Factors affecting release of 3H-dopamine from perfused carp retina

The Effects of Amfonelic Acid and Some Other Central Stimulants on Mouse Striatal Tyramine, Dopamine and Homovanillic Acid

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Nomifensine: a new potent inhibitor of dopamine uptake into synaptosomes from rat brain corpus striatum

Cited by 295 publications

References 7 publications

False labelling of dopaminergic terminals in the rabbit caudate nucleus: uptake and release of [3H]‐5‐hydroxytryptamine

False labelling of dopaminergic terminals in the rabbit caudate nucleus: uptake and release of [3H]‐5‐hydroxytryptamine

Factors affecting release of 3H-dopamine from perfused carp retina

The Effects of Amfonelic Acid and Some Other Central Stimulants on Mouse Striatal Tyramine, Dopamine and Homovanillic Acid

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False labelling of dopaminergic terminals in the rabbit caudate nucleus: uptake and release of [³H]‐5‐hydroxytryptamine

False labelling of dopaminergic terminals in the rabbit caudate nucleus: uptake and release of [³H]‐5‐hydroxytryptamine