EVIDENCE CONCERNING THE INVOLVEMENT OF 5‐HYDROXYTRYPTAMINE IN THE LOCOMOTOR ACTIVITY PRODUCED BY AMPHETAMINE OR TRANYLCYPROMINE PLUS <scp>l</scp>‐DOPA

Green, A.R.; Kelly, Peter H.

doi:10.1111/j.1476-5381.1976.tb07664.x

Cited by 53 publications

(22 citation statements)

References 38 publications

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“…The effect of depleting brain 5-hydroxytryptamine with p-chloroamphetamine on the behaviour produced by tranylcypromine and L-DOPA The original findings of Green & Kelly (1976) were confirmed and it was observed that all the behavioural changes such as forepaw treading and head weaving were still present in animals pretreated with p-chloroamphetamine (Figure 3). Furthermore these changes were still present 90 min after L-DOPA administration and did not diminish as might be expected if residual 5-HT were being further depleted.…”

Section: Resultssupporting

confidence: 61%

“…Consequently the activity counts were increased although produced by a radically different behaviour in the methysergide and methergoline pretreated rats. Administration of either p-chloroamphetamine or tranylcypromine and tryptamine results in the appearance of syndromes indistinguishable from those seen after tranylcypromine and L-tryptophan and there is evidence that these syndromes also result from release of brain 5-hydroxytryptaminergic systems (Foldes & Costa, 1975;Jacobs, 1976;Green & Kelly, 1976). These syndromes were affected by Lesioning of the spinal cord 5-HT tracts by discrete injection of 5,7-DHT resulted in an enhanced behavioural response to the 5-HT agonist, 5-MeODMT, which is consistent with the view of Jacobs & Klemfuss (1975) that the syndrome is predominantly mediated by spinal 5-HT systems and with other evidence that 5-HT receptors become supersensitive on denervation (Trulson et al, 1976;Hole, Fuxe & Johnson, 1976).…”

Section: Discussionmentioning

confidence: 99%

“…A similar behavioural syndrome follows administration of a MAO inhibitor and L-DOPA, and this behaviour has been used as an index of dopaminergic function (Everett, Weigland & Rinaldi, 1963;Green & Kelly, 1976). The similarity of the two behavioural syndromes suggests they may have a common neurochemical basis.…”

Section: Introductionmentioning

confidence: 99%

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The Effects of Putative 5‐hydroxytryptamine Antagonists on the Behaviour Produced by Administration of Tranylcypromine and L‐tryptophan or Tranylcypromine and L‐dopa to Rats

Deakin

Green

1978

British J Pharmacology

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147

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1 The putative 5-hydroxytryptamine (5-HT) receptor blocking drugs methysergide (10 mg/kg) and methergoline (5 mg/kg) were found to abolish some components of the hyperactivity syndrome, including head weaving and forepaw treading, which follow administration to rats of tranylcypromine (20 mg/kg) and L-tryptophan (100 mg/kg). Hyperactivity and hyper-reactivity were potentiated with a resultant increase in automated locomotor activity counts. In contrast (-)-propranolol (20 mg/kg) inhibited all features of the syndrome. The same results were obtained with these drugs when the behaviour was elicited by p-chloroamphetamine (10 mg/kg) or by tranylcypromine and tryptamine (10 mg/kg).2 Methysergide and methergoline had similar effects on the syndrome produced by tranylcypromine and L-DOPA (50 mg/kg) whereas propranolol was without effect. 3 None of the putative 5-HT receptor antagonists affected brain 5-HT turnover as assessed by rate of accumulation of 5-HT following monoamine oxidase inhibition with tranylcypromine. 4 Microinjections of 5,7-dihydroxytryptamine into the spinal cord resulted in a 70% fall in cord 5-HT concentrations without an effect on brain 5-HT concentrations. The behavioural response to the putative 5-HT receptor agonist, 5-methoxy N,N-dimethyltryptamine (2 mg/kg), was potentiated in these animals suggesting that 5-HT receptors become supersensitive on denervation, and that some components of the behavioural syndrome are mediated by spinal cord 5-HT receptors. 5 Pretreatment with a-methyl p-tyrosine (2 x 200 mg/kg) delayed the onset of all components of the behaviour elicited by tranylcypromine/L-tryptophan by 60 min, indicating an involvement of catecholamines in the syndrome. 6 p-Chloroamphetamine-induced 5-HT depletion had no effect on any component of the tranylcypromine-L-DOPA behaviour.

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Section: Resultssupporting

confidence: 61%

Section: Discussionmentioning

confidence: 99%

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The Effects of Putative 5‐hydroxytryptamine Antagonists on the Behaviour Produced by Administration of Tranylcypromine and L‐tryptophan or Tranylcypromine and L‐dopa to Rats

Deakin

Green

1978

British J Pharmacology

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147

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“…To do this, both biochemical measurements and a behavioural model have been used in an analagous way to the previous study on 5-HT. The behaviour studied was that of the locomotor activity which follows administration of an MAO inhibitor and L-3,4-dihydroxyphenylalanine (L-DOPA) and which has been shown to be the result of increasing dopamine concentrations in the brain (Everett, Wiegland & Rinaldi, 1963;Everett, 1966;Green & Kelly, 1976).…”

Section: Introductionmentioning

confidence: 99%

“…Behavioural changes following the L-DOPA administration were exactly as described by Green & Kelly (1976).…”

Section: Introductionmentioning

confidence: 99%

EVIDENCE FOR DOPAMINE DEAMINATION BY BOTH TYPE A AND TYPE B MONOAMINE OXIDASE IN RAT BRAIN in vivo AND FOR THE DEGREE OF INHIBITION OF ENZYME NECESSARY FOR INCREASED FUNCTIONAL ACTIVITY OF DOPAMINE AND 5‐HYDROXYTRYPTAMINE

Green¹,

Mitchell²,

Tordoff³

et al. 1977

British J Pharmacology

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149

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1 Tranylcypromine (20 mg/kg) administration to rats totally inhibited brain monoamine oxidase (MAO) oxidation of 5-hydroxytryptamine (5-HT), phenylethylamine and dopamine as measured in vitro. When L-3,4-dihydroxyphenylalanine (L-DOPA) (50 mg/kg) was given 30 min after the tranylcypromine, brain dopamine and noradrenaline concentrations rose markedly and the rats displayed characteristic behavioural changes and locomotor activity. 2 Clorgyline (5 mg/kg) administration inhibited 5-HT oxidation by almost 100% but phenylethylamine by only 29% while (-)-deprenil (5 mg/kg) injection almost totally inhibited phenylethylamine oxidation and inhibited 5-HT metabolism by only 31%. Administration of L-DOPA after pretreatment with either drug did not alter brain dopamine or noradrenaline concentrations and the animals did not display any behavioural changes.3 Administration of clorgyline plus (-)-deprenil (5 mg/kg of each) almost totally inhibited oxidation of both phenylethylamine and 5-HT; there was a large rise of brain dopamine and noradrenaline concentrations and the animals displayed the behavioural changes observed when tranylcypromine and L-DOPA had been given. 4 The effects of tranylcypromine (20 mg/kg) on brain 5-HT, dopamine and noradrenaline concentrations up to 48 h after injection were recorded. Brain 5-HT concentrations were considerably elevated for 18 h after injection and then fell steadily. In contrast, brain dopamine concentrations rose slightly and remained at this level for 48 h while noradrenaline levels doubled and also remained at this level for 48 hours.S When L-tryptophan (50 mg/kg) was given at various times after tranylcypromine the characteristic hyperactivity syndrome appeared at 12 h but not 18 h after tranylcypromine and a further rise in brain 5-HT was only observed at 12 hours. When L-DOPA (50 mg/kg) was given at various times after tranylcypromine a further large rise in brain dopamine and noradrenaline occurred at 12 h but not at 18 h and all the behavioural changes were observed only at 12 hours. 6 Measurement of MAO activity at the above times after tranylcypromine showed that the half-life of recovery of the enzyme activity with 5-HT and dopamine as substrates was 4.5 days and 8.5 days with phenylethylamine as substrate. Inhibition of MAO oxidation of dopamine and 5-HT was approximately 85%, 18 h after tranylcypromine injection. 7 It is concluded from both the studies with clorgyline and deprenil and the recovery of MAO activity after tranylcypromine, that dopamine is metabolized by both Type A and Type B MAO in vivo and that it is only when both forms are almost totally inhibited that there is an increase in dopamine and 5-HT functional activity, as judged by the appearance of the hyperactivity syndromes.

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Biogenic Monoamine Metabolism and Functional Activity in Iron‐Deficient Rats: Behavioural Correlates

Youdim¹,

Green²

1977

Novartis Foundation Symposia

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EVIDENCE CONCERNING THE INVOLVEMENT OF 5‐HYDROXYTRYPTAMINE IN THE LOCOMOTOR ACTIVITY PRODUCED BY AMPHETAMINE OR TRANYLCYPROMINE PLUS l‐DOPA

Cited by 53 publications

References 38 publications

The Effects of Putative 5‐hydroxytryptamine Antagonists on the Behaviour Produced by Administration of Tranylcypromine and L‐tryptophan or Tranylcypromine and L‐dopa to Rats

The Effects of Putative 5‐hydroxytryptamine Antagonists on the Behaviour Produced by Administration of Tranylcypromine and L‐tryptophan or Tranylcypromine and L‐dopa to Rats

EVIDENCE FOR DOPAMINE DEAMINATION BY BOTH TYPE A AND TYPE B MONOAMINE OXIDASE IN RAT BRAIN in vivo AND FOR THE DEGREE OF INHIBITION OF ENZYME NECESSARY FOR INCREASED FUNCTIONAL ACTIVITY OF DOPAMINE AND 5‐HYDROXYTRYPTAMINE

Biogenic Monoamine Metabolism and Functional Activity in Iron‐Deficient Rats: Behavioural Correlates

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