Brain-derived neurotrophic factor restores synaptic plasticity in a knock-in mouse model of Huntington's disease.

Brain-derived neurotrophic factor restores synaptic plasticity in a knock-in mouse model of Huntington's disease. Research Abstract Details 

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Brain-derived neurotrophic factor restores synaptic plasticity in a knock-in mouse model of Huntington's disease. Abstract Text:

Gary Lynch,Eniko A Kramar,Christopher S Rex,Yousheng Jia,Danielle Chappas,Christine M Gall,Danielle A Simmons,

Asymptomatic Huntington's disease (HD) patients exhibit memory and cognition deficits that generally worsen with age. Similarly, long-term potentiation (LTP), a form of synaptic plasticity involved in memory encoding, is impaired in HD mouse models well before motor disturbances occur. The reasons why LTP deteriorates are unknown. Here we show that LTP is impaired in hippocampal slices from presymptomatic Hdh(Q92) and Hdh(Q111) knock-in mice, describe two factors contributing to this deficit, and establish that potentiation can be rescued with brain-derived neurotrophic factor (BDNF). Baseline physiological measures were unaffected by the HD mutation, but LTP induction and, to a greater degree, consolidation were both defective. The facilitation of burst responses that normally occurs during a theta stimulation train was reduced in HD knock-in mice, as was theta-induced actin polymerization in dendritic spines. The decrease in actin polymerization and deficits in LTP stabilization were reversed by BDNF, concentrations of which were substantially reduced in hippocampus of both Hdh(Q92) and Hdh(Q111) mice. These results suggest that the HD mutation discretely disrupts processes needed to both induce and stabilize LTP, with the latter effect likely arising from reduced BDNF expression. That BDNF rescues LTP in HD knock-in mice suggests the possibility of treating cognitive deficits in asymptomatic HD gene carriers by upregulating production of the neurotrophin.

Brain-derived neurotrophic factor restores synaptic plasticity in a knock-in mouse model of Huntington's disease. Publishing Authors By Initials

G Lynch,EA Kramar,CS Rex,Y Jia,D Chappas,CM Gall,DA Simmons,

For similar diagnosis: diagnostic techniques and procedures: diagnostic techniques, neurological: electroencephalography: theta rhythm research abstracts see: diagnosis: diagnostic techniques and procedures: diagnostic techniques, neurological: electroencephalography: theta rhythm research

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Brain-derived neurotrophic factor restores synaptic plasticity in a knock-in mouse model of Huntington's disease. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The Journal of neuroscience : the official journal

VOLUME: 27

Page Numbers: 4424-34

Journal Abbreviation:

ISSN: 1529-2401

DAY: 18

MONTH: Apr

YEAR: 2007

Brain-derived neurotrophic factor restores synaptic plasticity in a knock-in mouse model of Huntington's disease. Information

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LANGUAGE: eng

NlmUniqueID: 8102140

Brain-derived neurotrophic factor restores synaptic plasticity in a knock-in mouse model of Huntington's disease. Keywords Mesh Terms:

KEYWORDS: Theta Rhythm

MESH TERMS: metabolism

Chemical & Substance for Abstract: Brain-derived neurotrophic factor restores synaptic plasticity in a knock-in mouse model of Huntington's disease. Information

Substance Name: Brain-Derived Neurotrophic Factor

Registry Number: 0

Grant and Affiliation Information for Brain-derived neurotrophic factor restores synaptic plasticity in a knock-in mouse model of Huntington's disease.

AFFILIATION: Department of Psychiatry and Human Behavior, University of California, Irvine, California 92617-4291, USA.

Country: United States

AGENCY: United States NINDS

GRANT: NS051823

ACRONYM: NS

MEDLINETA: J Neurosci

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