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Tytuł pozycji:

Impaired long-term potentiation in the prefrontal cortex of Huntington's disease mouse models: rescue by D1 dopamine receptor activation.

Tytuł :
Impaired long-term potentiation in the prefrontal cortex of Huntington's disease mouse models: rescue by D1 dopamine receptor activation.
Autorzy :
Dallérac GM; Huntington's Disease Research Forum, Department of Life Sciences, The Open University, Milton Keynes, UK.
Vatsavayai SC
Cummings DM
Milnerwood AJ
Peddie CJ
Evans KA
Walters SW
Rezaie P
Hirst MC
Murphy KP
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Źródło :
Neuro-degenerative diseases [Neurodegener Dis] 2011; Vol. 8 (4), pp. 230-9. Date of Electronic Publication: 2011 Feb 01.
Typ publikacji :
Journal Article; Research Support, Non-U.S. Gov't
Język :
English
Imprint Name(s) :
Original Publication: Basel : Karger, c2004-
MeSH Terms :
Huntington Disease/*physiopathology
Long-Term Potentiation/*physiology
Prefrontal Cortex/*physiopathology
Receptors, Dopamine D1/*metabolism
Animals ; Disease Models, Animal ; Dopamine Agonists/pharmacology ; Electrophysiology ; Female ; Immunohistochemistry ; Long-Term Potentiation/drug effects ; Male ; Mice ; Mice, Transgenic ; Organ Culture Techniques ; Prefrontal Cortex/drug effects ; Synaptic Transmission/physiology
Substance Nomenclature :
0 (Dopamine Agonists)
0 (Receptors, Dopamine D1)
Entry Date(s) :
Date Created: 20110202 Date Completed: 20111013 Latest Revision: 20110510
Update Code :
20210210
DOI :
10.1159/000322540
PMID :
21282937
Czasopismo naukowe
Background: The introduction of gene testing for Huntington's disease (HD) has enabled the neuropsychiatric and cognitive profiling of human gene carriers prior to the onset of overt motor and cognitive symptoms. Such studies reveal an early decline in working memory and executive function, altered EEG and a loss of striatal dopamine receptors. Working memory is processed in the prefrontal cortex and modulated by extrinsic dopaminergic inputs.
Objective: We sought to study excitatory synaptic function and plasticity in the medial prefrontal cortex of mouse models of HD.
Methods: We have used 2 mouse models of HD, carrying 89 and 116 CAG repeats (corresponding to a preclinical and symptomatic state, respectively) and performed electrophysiological field recording in coronal slices of the medial prefrontal cortex.
Results: We report that short-term synaptic plasticity and long-term potentiation (LTP) are impaired and that the severity of impairment is correlated with the size of the CAG repeat. Remarkably, the deficits in LTP and short-term plasticity are reversed in the presence of a D(1) dopamine receptor agonist (SKF38393).
Conclusion: In a previous study, we demonstrated that a deficit in long-term depression (LTD) in the perirhinal cortex could also be reversed by a dopamine agonist. These and our current data indicate that inadequate dopaminergic modulation of cortical synaptic function is an early event in HD and may provide a route for the alleviation of cognitive dysfunction.
(Copyright © 2011 S. Karger AG, Basel.)

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