Restoration of synaptic plasticity in the host striatum: can transplants make it?
Rylander, Daniella LU
(2013)
In NeuroReport
- Abstract
- Intrastriatal transplantation of dopamine (DA) neurons can restore DA levels in the striatum and improve parkinsonian deficits in experimental studies. However, the mechanisms underlying these effects are poorly understood. Corticostriatal synaptic plasticity represents an important cellular mechanism for information storage and behavioural learning in the brain. This mechanism is defective in Parkinson's disease (PD). Indeed, the lack of endogenous DA innervation to the striatum causes morphological and functional rearrangements that are associated with altered synaptic plasticity in the corticostriatal pathway. In turn, malfunctioning synaptic plasticity is associated with motor deficits that resemble features of PD. It is yet unknown... (More)
- Intrastriatal transplantation of dopamine (DA) neurons can restore DA levels in the striatum and improve parkinsonian deficits in experimental studies. However, the mechanisms underlying these effects are poorly understood. Corticostriatal synaptic plasticity represents an important cellular mechanism for information storage and behavioural learning in the brain. This mechanism is defective in Parkinson's disease (PD). Indeed, the lack of endogenous DA innervation to the striatum causes morphological and functional rearrangements that are associated with altered synaptic plasticity in the corticostriatal pathway. In turn, malfunctioning synaptic plasticity is associated with motor deficits that resemble features of PD. It is yet unknown whether or not transplanted dopaminergic neurons can restore these striatal deficits in PD. Could this be the mechanism underlying the therapeutic effects of transplants? Recent studies have begun to shed light on this matter using different approaches. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/4143052
- author
- Rylander, Daniella
LU
- organization
- publishing date
- 2013-10-22
- type
- Contribution to journal
- publication status
- published
- subject
- in
- NeuroReport
- publisher
- Lippincott Williams & Wilkins
- external identifiers
-
- pmid:24152765
- wos:000330375600005
- scopus:84889248236
- pmid:24152765
- ISSN
- 1473-558X
- DOI
- 10.1097/WNR.0000000000000061
- language
- English
- LU publication?
- yes
- id
- 906cb38b-0b44-4f0f-a009-2f9b15b80717 (old id 4143052)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/24152765?dopt=Abstract
- date added to LUP
- 2016-04-01 09:56:27
- date last changed
- 2024-01-06 03:43:51
@article{906cb38b-0b44-4f0f-a009-2f9b15b80717,
abstract = {{Intrastriatal transplantation of dopamine (DA) neurons can restore DA levels in the striatum and improve parkinsonian deficits in experimental studies. However, the mechanisms underlying these effects are poorly understood. Corticostriatal synaptic plasticity represents an important cellular mechanism for information storage and behavioural learning in the brain. This mechanism is defective in Parkinson's disease (PD). Indeed, the lack of endogenous DA innervation to the striatum causes morphological and functional rearrangements that are associated with altered synaptic plasticity in the corticostriatal pathway. In turn, malfunctioning synaptic plasticity is associated with motor deficits that resemble features of PD. It is yet unknown whether or not transplanted dopaminergic neurons can restore these striatal deficits in PD. Could this be the mechanism underlying the therapeutic effects of transplants? Recent studies have begun to shed light on this matter using different approaches.}},
author = {{Rylander, Daniella}},
issn = {{1473-558X}},
language = {{eng}},
month = {{10}},
publisher = {{Lippincott Williams & Wilkins}},
series = {{NeuroReport}},
title = {{Restoration of synaptic plasticity in the host striatum: can transplants make it?}},
url = {{http://dx.doi.org/10.1097/WNR.0000000000000061}},
doi = {{10.1097/WNR.0000000000000061}},
year = {{2013}},
}