Restoration of synaptic plasticity in the host striatum: can transplants make it?
Author
Summary, in English
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.
Department/s
Publishing year
2013-10-22
Language
English
Publication/Series
NeuroReport
Links
Document type
Journal article
Publisher
Lippincott Williams & Wilkins
Topic
- Neurosciences
Status
Published
Research group
- Basal Ganglia Pathophysiology
ISBN/ISSN/Other
- ISSN: 1473-558X