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Effect of prostaglandin E2 on central and peripheral catecholamine neurons

1973; Elsevier BV; Volume: 21; Issue: 3 Linguagem: Inglês

10.1016/0014-2999(73)90139-8

1879-0712

Sune Bergström, Lars‐Ove Farnebo, Kjell Fuxé,

Neuroscience and Neuropharmacology Research

Effects of prostaglandin E2 (PGE2) on catecholamine (CA) release from CA neurons have been studied in two models; influence on field stimulation-induced overflow of tritium from isolated tissues pre-incubated with 3H-CA; influence on dopamine (DA) disappearance in the neostriatum induced by tyrosine hydroxylase inhibition utilizing histochemical fluorescence analysis of catecholamines. In vitro PGE2 (3 × 10−6 M) caused a small but probably significant reduction of the field stimulation-induced tritium overflow from central noradrenaline (NA) and central DA nerve terminals and a significant reduction of the stimulation-induced overflow from peripheral NA nerve terminals. In the in vivo experiments PGE2 in μg amounts was dissolved in Krebs-Ringer bicarbonate buffer and infused into the left neostriatum, whereas buffer alone was infused into the right neostriatum. Infusion of 9–18 μg of PGE2 reduced the disappearance of DA fluorescence after treatment with the tyrosine hydroxylase inhibitor α-methyl-tyrosine methylester (H4468) under resting conditions, but could not counteract the increase in H4468-induced DA disappearance caused by electrical stimulation of the nigro-neostriatal DA pathway. The findings suggest that PGE2 can modify but not stop the release of DA and NA from central CA nerve terminals and indicate that prostaglandins might act as modulators of central CA neurotransmission.