Corticostriatal synaptic plasticity alterations in the R6/1 transgenic mouse model of Huntington's disease.
dopamine-dependent plasticity
dorsolateral striatum
polyglutamine (polyQ) diseases
spiny projection neurons
Journal
Journal of neuroscience research
ISSN: 1097-4547
Titre abrégé: J Neurosci Res
Pays: United States
ID NLM: 7600111
Informations de publication
Date de publication:
12 2019
12 2019
Historique:
received:
17
05
2019
revised:
13
08
2019
accepted:
20
08
2019
pubmed:
10
9
2019
medline:
22
8
2020
entrez:
10
9
2019
Statut:
ppublish
Résumé
Huntington's disease (HD) is a genetic neurodegenerative condition characterized by abnormal dopamine (DA)-glutamate interactions, severe alterations in motor control, and reduced behavioral flexibility. Experimental models of disease show that during symptomatic phases, HD shares with other hyperkinetic disorders the loss of synaptic depotentiation in the striatal spiny projection neurons (SPNs). Here we test the hypothesis that corticostriatal long-term depression (LTD), a well-conserved synaptic scaling down response to environmental stimuli, is also altered in symptomatic male R6/1 mice, a HD model with gradual development of symptoms. In vitro patch-clamp and intracellular recordings of corticostriatal slices from R6/1 mice confirm that, similar to other models characterized by hyperkinesia and striatal DA D1 receptor pathway dysregulation, once long-term potentiation (LTP) is induced, synaptic depotentiation is lost. Our new observations show that activity-dependent LTD was abolished in SPNs of mutant mice. In an experimental condition in which N-methyl-d-aspartate (NMDA) receptors are normally not recruited, in vitro bath application of DA revealed an abnormal response of D1 receptors that caused a shift in synaptic plasticity direction resulting in an NMDA-dependent LTP. Our results demonstrate that corticostriatal LTD is lost in R6/1 mouse model and confirm the role of aberrant DA-glutamate interactions in the alterations of synaptic scaling down associated with HD symptoms.
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1655-1664Informations de copyright
© 2019 Wiley Periodicals, Inc.
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