Serotonin-dopamine interaction in the induction and maintenance of L-DOPA-induced dyskinesias.
Appearance of dyskinesia is a common problem of long-term Levodopa (L-DOPA) treatment in Parkinson's disease (PD) patients and represents a major limitation for the pharmacological management of the motor symptoms in the advanced stages of disease. An increasing body of evidence points to dopamine released as a false neurotransmitter from the striatal serotonin terminals as the main pre-synaptic determinant of L-DOPA-induced dyskinesia. Here we review the animal experimental and human clinical data in support of this view, which point to the serotonin system as a promising target for anti-dyskinetic therapy in PD patients under L-DOPA medication.
Carta
Manolo
M
Neurobiology Unit, Wallenberg Neuroscience Center, Department of Experimental Medical Science, Lund University, Lund, Sweden. Manolo.Carta@med.lu.se
Carlsson
Thomas
T
Muñoz
Ana
A
Kirik
Deniz
D
Björklund
Anders
A
D000818:Animals; D002986:Clinical Trials as Topic; D004298:Dopamine / Q000378:metabolism*; D004409:Dyskinesia, Drug-Induced / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D007980:Levodopa / Q000009:adverse effects*; D010300:Parkinson Disease / Q000188:drug therapy* / Q000503:physiopathology; D020734:Parkinsonian Disorders / Q000378:metabolism / Q000503:physiopathology; D017729:Presynaptic Terminals / Q000378:metabolism; D020033:Protein Isoforms / Q000378:metabolism; D011954:Receptors, Dopamine / Q000378:metabolism; D011985:Receptors, Serotonin / Q000378:metabolism; D012701:Serotonin / Q000378:metabolism*
D020033:Protein Isoforms; D011954:Receptors, Dopamine; D011985:Receptors, Serotonin; D012701:Serotonin; D007980:Levodopa; D004298:Dopamine