Receptor activity and turnover of dopamine and noradrenaline after neuroleptics

Andén, Nils‐Erik; Butcher, Sherrel G.; Corrodi, H.; Fuxé, Kjell; Ungerstedt, Urban

doi:10.1016/0014-2999(70)90006-3

Cited by 1,020 publications

(150 citation statements)

References 29 publications

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“…Further evidence that the effects of bromocriptine are mediated by stimulation of dopamine receptors is that the induction of stereotyped behaviour and contralateral turning was inhibited by pimozide, a dopamine receptor blocking agent (Anden, Butcher, Corrodi, Fuxe & Ungerstedt, 1970). Corrodi et al, 1973, have also reported that the turning induced by bromocriptine in rats lesioned by the method of Ungerstedt (1971), is inhibited by prior administration of pimozide, as is the stimulation of locomotor activity by bromocriptine in mice (Johnson, Loew & Vigouret, in preparation).…”

Section: Discussionmentioning

confidence: 99%

STIMULANT PROPERTIES OF BROMOCRIPTINE ON CENTRAL DOPAMINE RECEPTORS IN COMPARISON TO APOMORPHINE, (+)‐AMPHETAMINE AND l‐DOPA

Johnson¹,

Loew²,

Vigouret³

1976

British J Pharmacology

209

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I The activity of bromocriptine has been investigated in tests for the stimulation of central dopaminergic mechanisms. The results obtained have been compared with those of apomorphine, (+)-amphetamine and L-DOPA. 2 Bromocriptine (2.5 to 10 mg/kg) induced stereotyped sniffing and licking in rats. The stereotypy was more intense than that induced by L-DOPA and less intense than that of apomorphine and (+)-amphetamine over the dose ranges studied. 3 In rats lesioned unilaterally in the substantia nigra by local injection of 6-hydroxydopamine, bromocriptine, like apomorphine and L-DOPA, induced turning contralateral to the side of the lesion. The smallest dose of bromocriptine to induce turning was 0.5 mg/kg. 4 Reserpine-induced catalepsy in mice was antagonized by bromocriptine, with an ED50 of 1.8 mg/kg. It was intermediate in potency to apomorphine and L-DOPA. 5Spontaneous locomotor activity in mice was stimulated by bromocriptine in a dose-dependent manner from 2.5 to 10 mg/kg after an initial suppression of activity. 6 In all experiments, bromocriptine was characterized by a prolonged duration of activity after a delay in the onset of effect. 7 The stereotyped behaviour induced by bromocriptine was inhibited by prior administration of pimozide, reserpine or a-methyl-p-tyrosine. 8 Bromocriptine-induced turning behaviour was abolished by pretreatment with pimozide, and reduced after a-methyl-p-tyrosine pretreatment. 9 The results obtained support the conclusion that bromocriptine acts by stimulating dopamine receptors in the central nervous system and that intact catecholamine synthesis and granular amine storage mechanisms are necessary for it to bring about its effects.

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Section: Discussionmentioning

confidence: 99%

STIMULANT PROPERTIES OF BROMOCRIPTINE ON CENTRAL DOPAMINE RECEPTORS IN COMPARISON TO APOMORPHINE, (+)‐AMPHETAMINE AND l‐DOPA

Johnson¹,

Loew²,

Vigouret³

1976

British J Pharmacology

209

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“…In the absence of pharmacological intervention, these cells typically have a bimodal spontaneous firing pattern: bursts Fwhich greatly enhance DA release in the NAcFfollowed by periods of quiescence, when DA release is low or absent, and high variability in the interspike interval (Gonon, 1988;Bean and Roth, 1991;. When noradrenergic transmission is blocked, both the excitatory and inhibitory effects of NE vanish, resulting in a regularization of DA neuron firing, and overall decreased DA utilization (Anden et al, 1970;Anden and Grabowska, 1976;Svensson, 1989, 1993;Zhou et al, 2006). This regularization is critical because, as Tassin, PuglisiAllegra, and others have shown, regularized DA release in the NAc is not functional in a behavioral sense; 'functional' DA release, which is characterized by the highly variable burst-quiescence pattern that is correlated with behavioral change, is largely dependent on a1AR activation (Darracq et al, 1998;Auclair et al, 2002).…”

Section: Control Of Dopamine Neuron Firing and Dopamine Release By Nementioning

confidence: 99%

There and Back Again: A Tale of Norepinephrine and Drug Addiction

Weinshenker

Schroeder

2006

Neuropsychopharmacol

319

277

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Fueled by anatomical, electrophysiological, and pharmacological analyses of endogenous brain reward systems, norepinephrine (NE) was identified as a key mediator of both natural and drug-induced reward in the late 1960s and early 1970s. However, reward experiments from the mid-1970s that could distinguish between the noradrenergic and dopaminergic systems resulted in the prevailing view that dopamine (DA) was the primary 'reward transmitter' (a belief holding some sway still today), thereby pushing NE into the background. Most damaging to the NE hypothesis of reward were studies demonstrating that NE receptor antagonists and NE reuptake inhibitors failed to impact drug self-administration. In recent years new tools, such as genetically engineered mice, and new experimental paradigms, such as reinstatement of drug seeking following withdrawal, have propelled NE back into the awareness of addiction researchers. Of particular interest is disulfiram, an inhibitor of the NE biosynthetic enzyme dopamine b-hydroxylase, which has demonstrated promising efficacy in the treatment of cocaine dependence in preliminary clinical trials. The purpose of this review is to synthesize the new data linking NE to critical aspects of DA signaling and drug addiction, with a focus on psychostimulants (eg, cocaine), opiates (eg, morphine), and alcohol.

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“…One commonly observed side-effect is the occurrence of drug-induced parkinsonian symptoms (Klawans, 1973). Both the antipsychotic action and the extrapyramidal parkinsonian side-effects of the neuroleptic drugs generally correlate well with their potency in blocking dopamine receptors as revealed by in vitro (Clement-Cormier, Kebabian, Petzold & Greengard, 1974;Horn, Cuello & Miller, 1974;Miller, Horn & Iversen, 1974) and in vivo (Anden, Butcher, Corrodi, Fuxe & Ungerstedt, 1970) models. However, it has been reported that some neuroleptics, notably thioridazine and clozapine, produce only minimal parkinsonian symptoms (Cole & Clyde, 1961;Burki, Ruch, Asper, Baggiolini & Stille, 1973) although they are potent blockers of dopamine effects in vitro ).…”

Section: Introductionmentioning

confidence: 99%

The Interaction of Neuroleptic and Muscarinic Agents With Central Dopaminergic Systems

Kelly¹,

Miller²

1975

British J Pharmacology

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1 The effect of muscarinic and neuroleptic agents on the turning behaviour induced by methamphetamine and apomorphine in rats with unilateral lesions of the substantia nigra induced by 6-hydroxydopamine has been examined. 2 Turning towards the side of the lesion induced by (+)-methamphetamine (5 mg/kg) was inhibited by a-flupenthixol (1 mg/kg) and a-clopenthixol (8 mg/kg) but not by high doses of their ,6-isomers. 3 Turning was inhibited by chlorpromazine (4 mg/kg) and pimozide (0.2 mg/kg). Thioridazine and clozapine (16 mg/kg) were ineffective. Turning in the same direction produced by scopolamine (10 mg/kg) was also inhibited by a-flupenthixol (1 mg/kg) and pimozide (0.25 mg/kg). 4 Tuming produced by methamphetamine (5 mg/kg) was inhibited by oxotremorine (0.75 mg/kg) even in the presence of methylatropine (5 mg/kg). 5 Tuming away from the side of the lesion induced by apomorphine (0.1 mg/kg) was inhibited by oxotremorine (0.75 mg/kg) but not by thioridazine or clozapine (16 mg/kg). 6 These results are discussed with regard to the mode of action of neuroleptic drugs in producing anti-psychotic effects and drug-induced Parkinsonism.

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Receptor activity and turnover of dopamine and noradrenaline after neuroleptics

Cited by 1,020 publications

References 29 publications

STIMULANT PROPERTIES OF BROMOCRIPTINE ON CENTRAL DOPAMINE RECEPTORS IN COMPARISON TO APOMORPHINE, (+)‐AMPHETAMINE AND l‐DOPA

STIMULANT PROPERTIES OF BROMOCRIPTINE ON CENTRAL DOPAMINE RECEPTORS IN COMPARISON TO APOMORPHINE, (+)‐AMPHETAMINE AND l‐DOPA

There and Back Again: A Tale of Norepinephrine and Drug Addiction

The Interaction of Neuroleptic and Muscarinic Agents With Central Dopaminergic Systems

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