Role of serotonin neurons in the induction of levodopa‐ and graft‐induced dyskinesias in Parkinson's disease
Identifieur interne : 001E60 ( Main/Merge ); précédent : 001E59; suivant : 001E61Role of serotonin neurons in the induction of levodopa‐ and graft‐induced dyskinesias in Parkinson's disease
Auteurs : Manolo Carta [Suède] ; Thomas Carlsson [Suède] ; Ana Mu Oz [Suède] ; Deniz Kirik [Suède] ; Anders Björklund [Suède]Source :
- Movement Disorders [ 0885-3185 ] ; 2010.
English descriptors
- KwdEn :
- 5‐HT1A receptor agonist, 5‐HT1B receptor agonist, Animals, Antiparkinson Agents (adverse effects), Disease Models, Animal, Dyskinesias (etiology), Dyskinesias (pathology), Humans, Levodopa (adverse effects), L‐dopa, Neurons (drug effects), Neurons (physiology), Parkinson Disease (therapy), Serotonin (metabolism), Transplants (adverse effects), dyskinesia, graft‐induced dyskinesia, serotonin.
- MESH :
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- adverse effects : Transplants.
- drug effects : Neurons.
- etiology : Dyskinesias.
- chemical , metabolism : Serotonin.
- pathology : Dyskinesias.
- physiology : Neurons.
- therapy : Parkinson Disease.
- Animals, Disease Models, Animal, Humans.
Abstract
Recent studies in animal models of Parkinson's disease (PD) have provided evidence that dopamine released from spared serotonin afferents can act as a trigger of dyskinetic movements induced by repetitive, low doses of levodopa. Serotonin neurons have the capacity to store and release dopamine synthesized from systemically administered levodopa. However, because of the lack of any autoregulatory feedback control, dopamine released from serotonin terminals results in excessive swings in extracellular dopamine levels after peripheral administration of levodopa. Such “dysregulated” release of levodopa‐derived dopamine is likely to be responsible for the appearance of the abnormal movements in levodopa‐primed animals. This mechanism may also play a role in the development of graft‐induced dyskinesias in patients that receive fetal neuron transplants, possibly due to the inclusion of serotonin neurons in the grafted ventral midbrain tissue, which contribute to maintain dopamine receptors of the denervated striatum in a supersensitive state. © 2010 Movement Disorder Society
Url:
DOI: 10.1002/mds.22792
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<front><div type="abstract" xml:lang="en">Recent studies in animal models of Parkinson's disease (PD) have provided evidence that dopamine released from spared serotonin afferents can act as a trigger of dyskinetic movements induced by repetitive, low doses of levodopa. Serotonin neurons have the capacity to store and release dopamine synthesized from systemically administered levodopa. However, because of the lack of any autoregulatory feedback control, dopamine released from serotonin terminals results in excessive swings in extracellular dopamine levels after peripheral administration of levodopa. Such "dysregulated" release of levodopa-derived dopamine is likely to be responsible for the appearance of the abnormal movements in levodopa-primed animals. This mechanism may also play a role in the development of graft-induced dyskinesias in patients that receive fetal neuron transplants, possibly due to the inclusion of serotonin neurons in the grafted ventral midbrain tissue, which contribute to maintain dopamine receptors of the denervated striatum in a supersensitive state.</div>
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