The effect of single and repeated administration of bromocriptine on monoamine metabolism in rat brain and [3H]spiroperidol binding to striatal membranes
Identifieur interne : 006667 ( Main/Curation ); précédent : 006666; suivant : 006668The effect of single and repeated administration of bromocriptine on monoamine metabolism in rat brain and [3H]spiroperidol binding to striatal membranes
Auteurs : V. Muradas [Espagne] ; E. Bazan [Espagne] ; J. J. Gervas [Espagne] ; M. A. Mena [Espagne] ; J. G. De Yebenes [Espagne, États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 1986.
English descriptors
- KwdEn :
- Animals, Biogenic Monoamines (metabolism), Brain (drug effects), Bromocriptine, Bromocriptine (pharmacology), Corpus Striatum (drug effects), Dopamine, Male, Monoamine metabolism, Rats, Rats, Inbred Strains, Receptors, Dopamine (drug effects), Serotonin, Spiperone (metabolism), Synaptic Membranes (drug effects), Tritium (diagnostic use).
- MESH :
- chemical , diagnostic use : Tritium.
- chemical , drug effects : Receptors, Dopamine.
- chemical , metabolism : Biogenic Monoamines, Spiperone.
- drug effects : Brain, Corpus Striatum, Synaptic Membranes.
- chemical , pharmacology : Bromocriptine.
- Animals, Male, Rats, Rats, Inbred Strains.
Abstract
Administration of a single high dose of bromocriptine decreased synthesis and release of dopamine and serotonin in several brain regions, most notably in the striatum. Bromocriptine modified the kinetics of [3H]spiroperidol binding to striatal membranes, but these changes were not prominent 2 h after injection when modifications of monoamine metabolism were evaluated. After injection of the same dose of bromocriptine daily for 10 days, the decrease in dopamine synthesis persisted, while other aspects of monoamine metabolism, presumably controlled by dopamine autoreceptors, returned to normal values. This adaptation was not caused by decreased blood levels of bromocriptine, since bromocriptine accumulated in plasma after repeated drug administration. This study provides evidence that different aspects of dopamine cell function, presumably controlled by autoreceptors, show different patterns of adaptation after chronic administration of dopamine agonists.
Url:
DOI: 10.1002/mds.870010204
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ISTEX:E4C23B017568FC9502EB927361D05CDDD9F12587Le document en format XML
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<series><title level="j">Movement Disorders</title>
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<pubPlace>Hoboken</pubPlace>
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<term>Biogenic Monoamines (metabolism)</term>
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<term>Bromocriptine</term>
<term>Bromocriptine (pharmacology)</term>
<term>Corpus Striatum (drug effects)</term>
<term>Dopamine</term>
<term>Male</term>
<term>Monoamine metabolism</term>
<term>Rats</term>
<term>Rats, Inbred Strains</term>
<term>Receptors, Dopamine (drug effects)</term>
<term>Serotonin</term>
<term>Spiperone (metabolism)</term>
<term>Synaptic Membranes (drug effects)</term>
<term>Tritium (diagnostic use)</term>
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<keywords scheme="MESH" type="chemical" qualifier="diagnostic use" xml:lang="en"><term>Tritium</term>
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<term>Spiperone</term>
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<term>Corpus Striatum</term>
<term>Synaptic Membranes</term>
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<front><div type="abstract" xml:lang="en">Administration of a single high dose of bromocriptine decreased synthesis and release of dopamine and serotonin in several brain regions, most notably in the striatum. Bromocriptine modified the kinetics of [3H]spiroperidol binding to striatal membranes, but these changes were not prominent 2 h after injection when modifications of monoamine metabolism were evaluated. After injection of the same dose of bromocriptine daily for 10 days, the decrease in dopamine synthesis persisted, while other aspects of monoamine metabolism, presumably controlled by dopamine autoreceptors, returned to normal values. This adaptation was not caused by decreased blood levels of bromocriptine, since bromocriptine accumulated in plasma after repeated drug administration. This study provides evidence that different aspects of dopamine cell function, presumably controlled by autoreceptors, show different patterns of adaptation after chronic administration of dopamine agonists.</div>
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