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Publication Detail
Lack of autoreceptor-mediated inhibitory control of dopamine release in striatal synaptosomes of D2 receptor-deficient mice.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    L'hirondel M, Chéramy A, Godeheu G, Artaud F, Saiardi A, Borrelli E, Glowinski J
  • Publication date:
  • Pagination:
    253, 262
  • Journal:
    Brain Res
  • Volume:
  • Issue:
  • Status:
  • Country:
  • Print ISSN:
  • PII:
  • Language:
  • Keywords:
    4-Aminopyridine, Amphetamine, Animals, Apomorphine, Autoreceptors, Benzopyrans, Cocaine, Corpus Striatum, Dopamine, Dopamine Agonists, Dopamine Uptake Inhibitors, Dose-Response Relationship, Drug, Fluoresceins, Male, Membrane Potentials, Mice, Mice, Inbred C57BL, Mice, Knockout, Mutation, Neural Inhibition, Oxazines, Potassium Chloride, Presynaptic Terminals, Quinpirole, Receptors, Dopamine D2, Synaptosomes, Tritium
Mouse purified striatal synaptosomes were used to study the release of newly synthesised [3H]-dopamine ([3H]-DA) or of previously taken up [3H]-DA. Quinpirole (QP, 10 microM), a D2/D3 dopaminergic agonist, was found to reduce the release of newly synthesised [3H]-DA with a larger amplitude when 4-aminopyridine (100 microM) instead than veratridine (1 microM) or potassium (25 mM) was used to evoke DA release. Among the different D2/D3 dopaminergic agonists tested R(-)-propylnorapomorphine (NPA) and quinpirole were the most potent. These compounds reduced, in a concentration-dependent manner, the 4-aminopyridine-evoked release of [3H]-DA previously taken up by synaptosomes (50% maximal inhibition). In contrast, the D3 agonist PD-128,907 had little effect even when used at 100 nM. The QP (100 nM)-induced response was completely antagonised by sulpiride (1 microM). Strikingly, the NPA (100 nM) and PD-128,907 (100 nM)-evoked responses were completely suppressed in D2 receptor-deficient mice. This data strongly suggest that only D2 but not D3 receptors are involved in the autoreceptor-mediated inhibition of the evoked release of [3H]-DA. Interestingly, while amphetamine-induced release of [3H]-DA was not modified, a slight reduction of [3H]-DA efflux induced by the dopamine (DA) uptake inhibitor cocaine was observed in D2 receptor-deficient mice.
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