The antiparkinsonian drug budipine stimulates the activity of aromatic L‐amino acid decarboxylase and enhances L‐DOPA‐induced dopamine release in rat substantia nigra
Identifieur interne : 001E55 ( Main/Exploration ); précédent : 001E54; suivant : 001E56The antiparkinsonian drug budipine stimulates the activity of aromatic L‐amino acid decarboxylase and enhances L‐DOPA‐induced dopamine release in rat substantia nigra
Auteurs : C. S. Biggs [Royaume-Uni] ; A. Fisher [Royaume-Uni] ; M. S. Starr [Royaume-Uni]Source :
- Synapse [ 0887-4476 ] ; 1998-11.
English descriptors
Abstract
The present study examined the effects of the antiparkinsonian drug budipine on dopamine synthesis and release from L‐DOPA in the substantia nigra of reserpine‐treated rats. Budipine (at 100 μM, but not 10 μM) applied by reverse dialysis to the nigra caused a small and significant rise in dopamine recovery in normal rats, but not in rats pretreated with reserpine (4 mg/kg i.p. for 18 hours) and α‐methyl‐p‐tyrosine (α‐MPT; 200 mg/kg i.p. for 1 hour to limit dopamine synthesis to L‐DOPA). L‐DOPA applied to the nigra by reverse dialysis in reserpine + α‐MPT‐treated rats, increased the recovery of dopamine when applied at 5 or 10 μM, but not at 2 μM. Coadministration of budipine (10 μM) significantly enhanced L‐DOPA‐induced dopamine (and DOPAC) release with 5 μM L‐DOPA, but not with 2 or 10 μM L‐DOPA. This potentiation was even more pronounced when the budipine concentration was raised to 100 μM (equivalent to approximately 10 μM extracellularly). Pretreating rats with budipine (5, 12.5, or 20 mg/kg i.p.) for 1 hour significantly raised the activity of the enzyme L‐aromatic amino acid decarboxylase in the striata and nigras of intact rats, as well as in rats pretreated with reserpine alone (5 mg/kg i.p.), without altering tissue levels of dopamine or its metabolites. 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. These actions of budipine may be related to its weak NMDA receptor antagonist property. Synapse 30:309–317, 1998. © 1998 Wiley‐Liss, Inc.
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DOI: 10.1002/(SICI)1098-2396(199811)30:3<309::AID-SYN8>3.0.CO;2-F
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Budipine (at 100 μM, but not 10 μM) applied by reverse dialysis to the nigra caused a small and significant rise in dopamine recovery in normal rats, but not in rats pretreated with reserpine (4 mg/kg i.p. for 18 hours) and α‐methyl‐p‐tyrosine (α‐MPT; 200 mg/kg i.p. for 1 hour to limit dopamine synthesis to L‐DOPA). L‐DOPA applied to the nigra by reverse dialysis in reserpine + α‐MPT‐treated rats, increased the recovery of dopamine when applied at 5 or 10 μM, but not at 2 μM. Coadministration of budipine (10 μM) significantly enhanced L‐DOPA‐induced dopamine (and DOPAC) release with 5 μM L‐DOPA, but not with 2 or 10 μM L‐DOPA. This potentiation was even more pronounced when the budipine concentration was raised to 100 μM (equivalent to approximately 10 μM extracellularly). Pretreating rats with budipine (5, 12.5, or 20 mg/kg i.p.) for 1 hour significantly raised the activity of the enzyme L‐aromatic amino acid decarboxylase in the striata and nigras of intact rats, as well as in rats pretreated with reserpine alone (5 mg/kg i.p.), without altering tissue levels of dopamine or its metabolites. 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. These actions of budipine may be related to its weak NMDA receptor antagonist property. Synapse 30:309–317, 1998. © 1998 Wiley‐Liss, Inc.</div></front></TEI><affiliations><list><country><li>Royaume-Uni</li></country></list><tree><country name="Royaume-Uni"><noRegion><name sortKey="Biggs, C S" sort="Biggs, C S" uniqKey="Biggs C" first="C. S." last="Biggs">C. S. 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