The role of pallidal serotonergic function in Parkinson's disease dyskinesias: a positron emission tomography study.
Smith, Ruben LU ; Wu, Kit ; Hart, Thomas ; Loane, Clare ; Brooks, David J ; Björklund, Anders LU
; Odin, Per
LU
; Piccini, Paola
and Politis, Marios
(2015)
In Neurobiology of Aging
36(4).
p.1736-1742
- Abstract
- We have investigated the role of globus pallidus (GP) serotonergic terminals in the development of levodopa-induced dyskinesias (LIDs) in Parkinson's disease (PD). We studied 12 PD patients without LIDs, 12 PD patients with LIDs, and 12 healthy control subjects. We used (11)C-DASB positron emission tomography (PET), a marker of serotonin transporter availability, and (11)C-raclopride PET to measure changes in synaptic dopamine levels following levodopa administration. PD patients without LIDs showed a significant reduction of GP serotonin transporter binding compared with healthy controls although this was within the normal range in PD patients with LIDs. Levels of GP serotonin transporter binding correlated positively with severity of... (More)
- We have investigated the role of globus pallidus (GP) serotonergic terminals in the development of levodopa-induced dyskinesias (LIDs) in Parkinson's disease (PD). We studied 12 PD patients without LIDs, 12 PD patients with LIDs, and 12 healthy control subjects. We used (11)C-DASB positron emission tomography (PET), a marker of serotonin transporter availability, and (11)C-raclopride PET to measure changes in synaptic dopamine levels following levodopa administration. PD patients without LIDs showed a significant reduction of GP serotonin transporter binding compared with healthy controls although this was within the normal range in PD patients with LIDs. Levels of GP serotonin transporter binding correlated positively with severity of dyskinesias. (11)C-raclopride PET detected a significant rise in GP synaptic dopamine levels of patients with LIDs after a levodopa challenge but not in patients with a stable response. Our findings indicate that LIDs in PD are associated with higher GP serotonergic function. This increased serotonin function may result in further dysregulation of thalamocortical signals and so promote the expression of dyskinesias. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/5145518
- author
- Smith, Ruben
LU
; Wu, Kit
; Hart, Thomas
; Loane, Clare
; Brooks, David J
; Björklund, Anders
LU
; Odin, Per
LU
; Piccini, Paola
and Politis, Marios
- organization
- publishing date
- 2015
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Neurobiology of Aging
- volume
- 36
- issue
- 4
- pages
- 1736 - 1742
- publisher
- Elsevier
- external identifiers
-
- pmid:25649022
- wos:000355095300014
- scopus:84925237392
- pmid:25649022
- ISSN
- 1558-1497
- DOI
- 10.1016/j.neurobiolaging.2014.12.037
- language
- English
- LU publication?
- yes
- id
- b40281d0-37a1-4f86-b444-1768959e0862 (old id 5145518)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/25649022?dopt=Abstract
- date added to LUP
- 2016-04-01 09:51:31
- date last changed
- 2022-12-09 17:28:50
@article{b40281d0-37a1-4f86-b444-1768959e0862,
abstract = {{We have investigated the role of globus pallidus (GP) serotonergic terminals in the development of levodopa-induced dyskinesias (LIDs) in Parkinson's disease (PD). We studied 12 PD patients without LIDs, 12 PD patients with LIDs, and 12 healthy control subjects. We used (11)C-DASB positron emission tomography (PET), a marker of serotonin transporter availability, and (11)C-raclopride PET to measure changes in synaptic dopamine levels following levodopa administration. PD patients without LIDs showed a significant reduction of GP serotonin transporter binding compared with healthy controls although this was within the normal range in PD patients with LIDs. Levels of GP serotonin transporter binding correlated positively with severity of dyskinesias. (11)C-raclopride PET detected a significant rise in GP synaptic dopamine levels of patients with LIDs after a levodopa challenge but not in patients with a stable response. Our findings indicate that LIDs in PD are associated with higher GP serotonergic function. This increased serotonin function may result in further dysregulation of thalamocortical signals and so promote the expression of dyskinesias.}},
author = {{Smith, Ruben and Wu, Kit and Hart, Thomas and Loane, Clare and Brooks, David J and Björklund, Anders and Odin, Per and Piccini, Paola and Politis, Marios}},
issn = {{1558-1497}},
language = {{eng}},
number = {{4}},
pages = {{1736--1742}},
publisher = {{Elsevier}},
series = {{Neurobiology of Aging}},
title = {{The role of pallidal serotonergic function in Parkinson's disease dyskinesias: a positron emission tomography study.}},
url = {{http://dx.doi.org/10.1016/j.neurobiolaging.2014.12.037}},
doi = {{10.1016/j.neurobiolaging.2014.12.037}},
volume = {{36}},
year = {{2015}},
}