Title : Role of endogenous dopamine in the central serotonergic deficits induced by 3,4-methylenedioxymethamphetamine.

Pub. Date : 1988 Oct

PMID : 2902215






10 Functional Relationships(s)
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1 Depletion of central dopamine content with alpha-methyl-p-tyrosine or reserpine, or selective destruction of nigrostriatal dopamine projections with bilateral 6-hydroxydopamine-induced substantia nigral lesions, partially blocked the immediate MDMA-induced reduction in rat striatal tryptophan hydroxylase (TPH) activity. Oxidopamine tryptophan hydroxylase 1 Rattus norvegicus
2 Depletion of central dopamine content with alpha-methyl-p-tyrosine or reserpine, or selective destruction of nigrostriatal dopamine projections with bilateral 6-hydroxydopamine-induced substantia nigral lesions, partially blocked the immediate MDMA-induced reduction in rat striatal tryptophan hydroxylase (TPH) activity. Oxidopamine tryptophan hydroxylase 1 Rattus norvegicus
3 In addition, the longer-term TPH deficits caused by a high single dose of MDMA were completely prevented by prior alpha-methyl-p-tyrosine or reserpine, and attenuated significantly by inhibition of dopamine uptake with the selective dopamine-uptake blocker GBR 12909. N-Methyl-3,4-methylenedioxyamphetamine tryptophan hydroxylase 1 Rattus norvegicus
4 In addition, the longer-term TPH deficits caused by a high single dose of MDMA were completely prevented by prior alpha-methyl-p-tyrosine or reserpine, and attenuated significantly by inhibition of dopamine uptake with the selective dopamine-uptake blocker GBR 12909. alpha-Methyltyrosine tryptophan hydroxylase 1 Rattus norvegicus
5 In addition, the longer-term TPH deficits caused by a high single dose of MDMA were completely prevented by prior alpha-methyl-p-tyrosine or reserpine, and attenuated significantly by inhibition of dopamine uptake with the selective dopamine-uptake blocker GBR 12909. Reserpine tryptophan hydroxylase 1 Rattus norvegicus
6 In addition, the longer-term TPH deficits caused by a high single dose of MDMA were completely prevented by prior alpha-methyl-p-tyrosine or reserpine, and attenuated significantly by inhibition of dopamine uptake with the selective dopamine-uptake blocker GBR 12909. Dopamine tryptophan hydroxylase 1 Rattus norvegicus
7 In addition, the longer-term TPH deficits caused by a high single dose of MDMA were completely prevented by prior alpha-methyl-p-tyrosine or reserpine, and attenuated significantly by inhibition of dopamine uptake with the selective dopamine-uptake blocker GBR 12909. Dopamine tryptophan hydroxylase 1 Rattus norvegicus
8 In addition, the longer-term TPH deficits caused by a high single dose of MDMA were completely prevented by prior alpha-methyl-p-tyrosine or reserpine, and attenuated significantly by inhibition of dopamine uptake with the selective dopamine-uptake blocker GBR 12909. glutathione-bicarbonate-Ringer solution tryptophan hydroxylase 1 Rattus norvegicus
9 These results implicate endogenous drug-released dopamine as a partial mediator of the initial decrease in TPH activity caused by MDMA and as an important prerequisite to the development of long-term MDMA-induced neurotoxicity. Dopamine tryptophan hydroxylase 1 Rattus norvegicus
10 These results implicate endogenous drug-released dopamine as a partial mediator of the initial decrease in TPH activity caused by MDMA and as an important prerequisite to the development of long-term MDMA-induced neurotoxicity. N-Methyl-3,4-methylenedioxyamphetamine tryptophan hydroxylase 1 Rattus norvegicus