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Role of Serotonin Neurons in L-DOPA- and Graft-Induced Dyskinesia in a Rat Model of Parkinson's Disease.

Shin, Eunju LU ; Tronci, Elisabetta and Carta, Manolo LU (2012) In Parkinson's Disease 2012(Jun 11).
Abstract
L-DOPA, the most effective drug to treat motor symptoms of Parkinson's disease, causes abnormal involuntary movements, limiting its use in advanced stages of the disease. An increasing body of evidence points to the serotonin system as a key player in the appearance of L-DOPA-induced dyskinesia (LID). In fact, exogenously administered L-DOPA can be taken up by serotonin neurons, converted to dopamine and released as a false transmitter, contributing to pulsatile stimulation of striatal dopamine receptors. Accordingly, destruction of serotonin fibers or silencing serotonin neurons by serotonin agonists could counteract LID in animal models. Recent clinical work has also shown that serotonin neurons are present in the caudate/putamen of... (More)
L-DOPA, the most effective drug to treat motor symptoms of Parkinson's disease, causes abnormal involuntary movements, limiting its use in advanced stages of the disease. An increasing body of evidence points to the serotonin system as a key player in the appearance of L-DOPA-induced dyskinesia (LID). In fact, exogenously administered L-DOPA can be taken up by serotonin neurons, converted to dopamine and released as a false transmitter, contributing to pulsatile stimulation of striatal dopamine receptors. Accordingly, destruction of serotonin fibers or silencing serotonin neurons by serotonin agonists could counteract LID in animal models. Recent clinical work has also shown that serotonin neurons are present in the caudate/putamen of patients grafted with embryonic ventral mesencephalic cells, producing intense serotonin hyperinnervation. These patients experience graft-induced dyskinesia (GID), a type of dyskinesia phenotypically similar to the one induced by L-DOPA but independent from its administration. Interestingly, the 5-HT(1A) receptor agonist buspirone has been shown to suppress GID in these patients, suggesting that serotonin neurons might be involved in the etiology of GID as for LID. In this paper we will discuss the experimental and clinical evidence supporting the involvement of the serotonin system in both LID and GID. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Parkinson's Disease
volume
2012
issue
Jun 11
publisher
Hindawi Publishing Corporation
external identifiers
  • wos:000324121600001
  • pmid:22762012
  • scopus:84863677359
ISSN
2042-0080
DOI
10.1155/2012/370190
language
English
LU publication?
yes
id
07d1f7ba-022b-4ec5-841e-a73e5673f08a (old id 2967486)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/22762012?dopt=Abstract
date added to LUP
2012-08-09 15:27:14
date last changed
2017-01-01 03:16:52
@article{07d1f7ba-022b-4ec5-841e-a73e5673f08a,
  abstract     = {L-DOPA, the most effective drug to treat motor symptoms of Parkinson's disease, causes abnormal involuntary movements, limiting its use in advanced stages of the disease. An increasing body of evidence points to the serotonin system as a key player in the appearance of L-DOPA-induced dyskinesia (LID). In fact, exogenously administered L-DOPA can be taken up by serotonin neurons, converted to dopamine and released as a false transmitter, contributing to pulsatile stimulation of striatal dopamine receptors. Accordingly, destruction of serotonin fibers or silencing serotonin neurons by serotonin agonists could counteract LID in animal models. Recent clinical work has also shown that serotonin neurons are present in the caudate/putamen of patients grafted with embryonic ventral mesencephalic cells, producing intense serotonin hyperinnervation. These patients experience graft-induced dyskinesia (GID), a type of dyskinesia phenotypically similar to the one induced by L-DOPA but independent from its administration. Interestingly, the 5-HT(1A) receptor agonist buspirone has been shown to suppress GID in these patients, suggesting that serotonin neurons might be involved in the etiology of GID as for LID. In this paper we will discuss the experimental and clinical evidence supporting the involvement of the serotonin system in both LID and GID.},
  articleno    = {370190},
  author       = {Shin, Eunju and Tronci, Elisabetta and Carta, Manolo},
  issn         = {2042-0080},
  language     = {eng},
  number       = {Jun 11},
  publisher    = {Hindawi Publishing Corporation},
  series       = {Parkinson's Disease},
  title        = {Role of Serotonin Neurons in L-DOPA- and Graft-Induced Dyskinesia in a Rat Model of Parkinson's Disease.},
  url          = {http://dx.doi.org/10.1155/2012/370190},
  volume       = {2012},
  year         = {2012},
}