Role of serotonin neurons in the induction of levodopa- and graft-induced dyskinesias in Parkinson's disease.

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Role of serotonin neurons in the induction of levodopa- and graft-induced dyskinesias in Parkinson's disease. / Carta, Manolo; Carlsson, Thomas; Munoz, Ana; Kirik, Deniz; Björklund, Anders.

I: Movement Disorders, Vol. 25 Suppl 1, 2010, s. S174-S179.

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

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T1 - Role of serotonin neurons in the induction of levodopa- and graft-induced dyskinesias in Parkinson's disease.

AU - Carta, Manolo

AU - Carlsson, Thomas

AU - Munoz, Ana

AU - Kirik, Deniz

AU - Björklund, Anders

PY - 2010

Y1 - 2010

N2 - 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.

AB - 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.

U2 - 10.1002/mds.22792

DO - 10.1002/mds.22792

M3 - Article

VL - 25 Suppl 1

SP - S174-S179

JO - Movement Disorders

JF - Movement Disorders

SN - 0885-3185

ER -