• Corpus ID: 8263046

Effects of the antiparkinsonian drug budipine on neurotransmitter release in central nervous system tissue in vitro.

@article{Jackisch1993EffectsOT,
  title={Effects of the antiparkinsonian drug budipine on neurotransmitter release in central nervous system tissue in vitro.},
  author={Rolf Jackisch and H. Y. Huang and Wolfgang Reimann and Norbert Limberger},
  journal={The Journal of pharmacology and experimental therapeutics},
  year={1993},
  volume={264 2},
  pages={
          889-98
        }
}
The effects of the antiparkinsonian drugs budipine and biperiden on spontaneous and electrically evoked release of dopamine (DA), acetylcholine (ACh), GABA or noradrenaline (NA) were studied in caudate nucleus or cortex slices, respectively, of the rabbit brain. Whereas both drugs (1-10 microM) strongly increased spontaneous [3H]outflow in caudate nucleus slices preincubated with [3H]DA, budipine inhibited but biperiden facilitated the evoked DA release. In the presence of the DA-reuptake… 
Effects of the antiparkinsonian drug budipine on central neurotransmitter systems.
TLDR
The present data suggest that budipine acts by blocking muscarinic and NMDA transmission while facilitation of dopaminergic transmission does not appear to contribute to its in vivo action.
The antiparkinsonian drugs budipine and biperiden are use-dependent (uncompetitive) NMDA receptor antagonists.
TLDR
It is concluded that budipine and biperiden are use-dependent (uncompetitive) antagonists at the NMDA receptor, binding to the receptor-linked ion channel, but probably not to the MK-801 binding site.
Properties of 3,4-diaminopyridine-evoked dopamine and acetylcholine release in rabbit caudate nucleus slices: involvement of facilitatory adenosine A2 receptors or nitric oxide?
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Multiple mechanisms of action: the pharmacological profile of budipine.
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  • Biology, Medicine
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  • 1999
TLDR
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Microdialysis study of the effects of the antiparkinsonian drug budipine on L‐DOPA‐induced release of dopamine and 5‐hydroxytryptamine by rat substantia nigra and corpus striatum
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It is concluded that budipine, at a therapeutically relevant dose, potentiates the release of dopamine newly synthesised from L‐DOPA from either end of the nigrostriatal dopamine axis.
Clinical efficacy of budipine in Parkinson's disease.
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Budipine induced a relevant additional positive effect in patients with an optimal dopaminergic therapy based on levodopa and dopamine agonists, such as bromocriptine, and that the long-term application of budipine may induce alevodopa-sparing effect.
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It is suggested that the beneficial effects of budipine, when used as an adjunct to L‐DOPA therapy of Parkinson's disease, may be due to an increase in the bioconversion of L‐ DOPA with a consequent rise in synaptic dopamine.
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Budipine, memantine and amantadine had similar effects against NMDA-induced currents in cultured hippocampal, cortical and superior colliculus neurones, although amantADine was somewhat more potent in cultured striatal neurones.
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