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• W2017995310 abstract "The effect of i.p. administered 5-hydroxytrptophan (5-HTP) on electroschock seizures and motility was studied in mice. High doses (600–2000 mg/kg) produced an anticonvulsant effect and hypermotility. Both effects were inhibited by the central decarboxylase inhibitor NSD 1015 (100 mg/kg i.p.) and potentiated by the peripheral decarboxylase inhibitor Ro 4-4602 (5 mg/kg i.p.). The catecholamine sysnthesis inhibitor α-methyl-p-tyrosine or H 4468 (100 and 200 mg/kg i.p.) did not alter the anticonvulsant effect but H 4468 (200 mg/kg i.p.). inhibited the hypermotility. Six inhibitors of neuronal NA and 5-HT uptake were administered orally at various times before 5-HTP (150 mg/kg), which alone was devoid of anticonvulsant effect and produced a weak hypermotility. Low doses of the selective 5-HT-uptake inhibitors paroxetine, fluoxetine and zimelidine potentiated both 5-HTP-induced effects. The selective NA uptake inhibitor protriptyline showed no or weak 5-HTP potentiation. These results indicate that the anticonvulsant effect of 5-HTP is dependent on increased synthesis and release of brain 5-HT. Both 5-HT and catecholamine release are presumably involved in mediating 5-HTP-induced hypermotility since selective 5-HT uptake inhibitors were the strongest potentiators of this behavior. Increased serotoninergic neurotransmission seems to play an important role." @default.
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• W2017995310 title "Potent and long-lasting potentiation of two 5-hydroxytryptophan-induced effects in mice by three selective 5-HT uptake inhibitors" @default.
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• W2017995310 doi "https://doi.org/10.1016/0014-2999(78)90243-1" @default.
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