Effect of amezinium on the release and catabolism of 3H-monoamines in brain slices

Steppeler, A.; Döring, C.; Hedler, L; Starke, Klaus

doi:10.1016/0006-2952(82)90535-4

Cited by 24 publications

(4 citation statements)

References 11 publications

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“…Electrically evoked overflow of [ 3 H] from brain slices preloaded with the appropriate marker is a valuable model for the study of the presynaptic modulation of action potential-induced, exocytotic neurotransmitter release (Birthelmer et al, 2003a,b ;Hertting et al, 1980 ;Jackisch et al, 1980). Conversely, the spontaneous [ 3 H] outflow from such slices (Ehret et al, 2001 ;Starke et al, 1981 ;Steppeler et al, 1982 ;Zumstein et al, 1981) and most probably also that induced by direct drug application mainly consists of a mixture of the efflux of both the [ 3 H] transmitter itself and its tritiated metabolites.…”

Section: Discussionmentioning

confidence: 99%

Effects of ethanol and 3,4-methylenedioxymethamphetamine (MDMA) alone or in combination on spontaneous and evoked overflow of dopamine, serotonin and acetylcholine in striatal slices of the rat brain

Riegert¹,

Wedekind²,

Hamida³

et al. 2008

Int. J. Neuropsychopharm.

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Ethanol (EtOH) potentiates the locomotor effects of 3,4-methylenedioxymetamphetamine (MDMA) in rats. This potentiation might involve pharmacokinetic and/or pharmacodynamic mechanisms. We explored whether the latter could be local. Using a slice superfusion approach, we assessed the effects of MDMA (0.3, 3microm) and/or EtOH (2mm) on the spontaneous outflow and electrically evoked release of serotonin (5-HT), dopamine (DA) and acetylcholine (ACh) in the striatum, and for comparison, on 5-HT release in hippocampal and neocortical tissue. MDMA and less effectively EtOH, augmented the outflow of 5-HT in all regions. The electrically evoked 5-HT release was increased by MDMA at 3microm in striatal slices only. With nomifensine throughout, EtOH significantly potentiated the 0.3microm MDMA-induced outflow of 5-HT, but only in striatal slices. EtOH or MDMA also enhanced the spontaneous outflow of DA, but MDMA reduced the electrically evoked DA release. With fluvoxamine throughout superfusion, EtOH potentiated the effect of MDMA on the spontaneous outflow of DA. Finally, 3microm MDMA diminished the electrically evoked release of ACh, an effect involving several receptors (D2, 5-HT2, NMDA, nicotinic, NK1), with some interactions with EtOH. Among other results, we show for the first time a local synergistic interaction of EtOH and MDMA on the spontaneous outflow of striatal DA and 5-HT, which could be relevant to the EtOH-induced potentiation of hyperlocomotion in MDMA-treated rats. These data do not preclude the contribution of other pharmacodynamic and/or pharmacokinetic mechanisms in vivo but support the hypothesis that EtOH may affect the abuse liability of MDMA.

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Section: Discussionmentioning

confidence: 99%

Effects of ethanol and 3,4-methylenedioxymethamphetamine (MDMA) alone or in combination on spontaneous and evoked overflow of dopamine, serotonin and acetylcholine in striatal slices of the rat brain

Riegert¹,

Wedekind²,

Hamida³

et al. 2008

Int. J. Neuropsychopharm.

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“…Separation of [3H]-5-HT from its metabolite [3H]-5-hydroxyindole acetic acid (5-HIAA) and of [3H]-dopamine from its deaminated metabolites in superfusate samples from caudate slices was performed using the separation method described by Steppeler et al (1982). The slices were electrically stimulated twice: the first stimulation was carried out in the absence of 6-nitroquipazine, whereas the 5-HT uptake blocker was added to the superfusion fluid from 55 min before the second stimulation until the end of superfusion.…”

Section: Superfusion Experimentsmentioning

confidence: 99%

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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“…Action poten-& ; Lenke, Gries & Kretzschmar, 1981; tials release it from the axons in a calcium-dependent, tetrodotoxin-sensitive manner . Amezinium is similarly transported into the noradrenergic neurones of rat brain (Steppeler, Doring, Hedler & Starke, 1982). The experiments described below show that, as in the periphery, previously taken-up [3H]-amezinium is released from occipitocortical preparations by electrical pulses, and that the stimulation-evoked overflow is blocked by tetrodotoxin as well as in calciumfree medium.…”

Section: Introductionmentioning

confidence: 76%

Release of [³H]‐amezinium from cortical noradrenergic axons: a model for the study of the α‐autoreceptor hypothesis

Hedler¹,

Starke²,

Steppeler³

1983

British J Pharmacology

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[3H]-amezinium is taken up selectively into noradrenergic axons and their transmitter-storing vesicles and is released from these axons by action potentials. We used it as a non-a-adrenergic marker in order to study the a-adrenergic autoinhibition of noradrenaline release.2 Rat occipitocortical slices were preincubated with [3H]-amezinium 0.03 tLM and then superfused and stimulated electrically (3 Hz for 3 min). The stimulation-evoked overflow of tritium was measured in six groups of slices: from saline-pretreated rats; from saline-pretreated rats, the slices being exposed to exogenous noradrenaline before preincubation with [3H]-amezinium; from saline-treated rats, slices from which were exposed simultaneously to noradrenaline and cocaine before preincubation with [3H]-amezinium; from rats in which noradrenaline stores had been depleted by pretreatment with a-methyltyrosine (a-NMT); from a-MT-treated rats, the slices being exposed to noradrenaline before preincubation with [3H]-amezinium; and from a-MT-treated rats, slices from which were exposed to noradrenaline plus cocaine before preincubation with [3H]-amezinium. 3 The stimulation-evoked overflow of tritium, expressed as a percentage of the tritium content of the tissue, was 1.15% in slices from saline-pretreated rats, and was similar in slices from salinepretreated rats after exposure to noradrenaline or noradrenaline plus cocaine. It was 2.56 % in slices from a-MT-treated rats, 1.20% from a-MT-treated rats after exposure to noradrenaline, and 2.88% from a-MT-treated rats after exposure to noradrenaline plus cocaine. 4 Yohimbine 0.1 and 1 piM increased the stimulation-evoked overflow of tritium in slices from all groups of saline-pretreated rats and in those slices from a-MT rats that had been in contact with exogenous noradrenaline. Yohimbine did not change the evoked overflow in slices from a-MT rats that had not been exposed to noradrenaline, or had been exposed to noradrenaline plus cocaine. 5 Clonidine 0.01-1 LM decreased the stimulation-evoked overflow of tritium moderately in slices from saline-pretreated rats, markedly in slices from a-MT-treated rats, and moderately again when the latter slices had been exposed to noradrenaline.6 It is concluded that the action potential-evoked release of [3H]-amezinium as well as the modulation of this release by yohimbine and clonidine depend on the presence or absence of a-adrenergic autoinhibition caused by the co-secretion of noradrenaline. When there is co-secretion of noradrenaline, the evoked release of [3H]-amezinium is relatively small, yohimbine increases the release, and clonidine can cause only moderate inhibition. When there is no or very little cosecretion of noradrenaline, the evoked release of [3H]-amezinium is at least doubled, yohimbine causes no further increase and clonidine produces strong inhibition.

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Effect of amezinium on the release and catabolism of 3H-monoamines in brain slices

Cited by 24 publications

References 11 publications

Effects of ethanol and 3,4-methylenedioxymethamphetamine (MDMA) alone or in combination on spontaneous and evoked overflow of dopamine, serotonin and acetylcholine in striatal slices of the rat brain

Effects of ethanol and 3,4-methylenedioxymethamphetamine (MDMA) alone or in combination on spontaneous and evoked overflow of dopamine, serotonin and acetylcholine in striatal slices of the rat brain

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

Release of [³H]‐amezinium from cortical noradrenergic axons: a model for the study of the α‐autoreceptor hypothesis

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Effect of amezinium on the release and catabolism of 3H-monoamines in brain slices

Cited by 24 publications

References 11 publications

Effects of ethanol and 3,4-methylenedioxymethamphetamine (MDMA) alone or in combination on spontaneous and evoked overflow of dopamine, serotonin and acetylcholine in striatal slices of the rat brain

Effects of ethanol and 3,4-methylenedioxymethamphetamine (MDMA) alone or in combination on spontaneous and evoked overflow of dopamine, serotonin and acetylcholine in striatal slices of the rat brain

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

Release of [3H]‐amezinium from cortical noradrenergic axons: a model for the study of the α‐autoreceptor hypothesis

Contact Info

Product

Resources

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

Release of [³H]‐amezinium from cortical noradrenergic axons: a model for the study of the α‐autoreceptor hypothesis