Multiple sources of striatal inhibition are differentially affected in Huntington's disease mouse models.
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Corticostriatal Dysfunction in Huntington's Disease: The BasicsOptogenetics for neurodegenerative diseases.Optogenetics: 10 years of microbial opsins in neuroscience.Genetic rescue of CB1 receptors on medium spiny neurons prevents loss of excitatory striatal synapses but not motor impairment in HD mice.Differential Alteration in Expression of Striatal GABAAR Subunits in Mouse Models of Huntington's DiseaseThe role for alterations in neuronal activity in the pathogenesis of polyglutamine repeat disorders.Altered excitatory and inhibitory inputs to striatal medium-sized spiny neurons and cortical pyramidal neurons in the Q175 mouse model of Huntington's disease.Forebrain deletion of the dystonia protein torsinA causes dystonic-like movements and loss of striatal cholinergic neurons.Enhanced GABAergic Inputs Contribute to Functional Alterations of Cholinergic Interneurons in the R6/2 Mouse Model of Huntington's DiseaseSelective expression of mutant huntingtin during development recapitulates characteristic features of Huntington's diseasePartial Amelioration of Peripheral and Central Symptoms of Huntington's Disease via Modulation of Lipid Metabolism.A small molecule TrkB ligand reduces motor impairment and neuropathology in R6/2 and BACHD mouse models of Huntington's disease.Hyperactivity and cortical disinhibition in mice with restricted expression of mutant huntingtin to parvalbumin-positive cells.Midbrain dopamine neurons sustain inhibitory transmission using plasma membrane uptake of GABA, not synthesis.Corticostriatal synaptic adaptations in Huntington's diseaseSelective Sparing of Striatal Interneurons after Poly (ADP-Ribose) Polymerase 1 Inhibition in the R6/2 Mouse Model of Huntington's Disease.Viral vector-based tools advance knowledge of basal ganglia anatomy and physiology.Unravelling and Exploiting Astrocyte Dysfunction in Huntington's Disease.Striatal Network Models of Huntington's Disease Dysfunction Phenotypes.Altered membrane properties and firing patterns of external globus pallidus neurons in the R6/2 mouse model of Huntington's disease.Expanding neurochemical investigations with multi-modal recording: simultaneous fast-scan cyclic voltammetry, iontophoresis, and patch clamp measurements.Changes in striatal activity and functional connectivity in a mouse model of Huntington's diseaseReduced tonic inhibition in striatal output neurons from Huntington mice due to loss of astrocytic GABA release through GAT-3.Optogenetic stimulation reveals distinct modulatory properties of thalamostriatal vs corticostriatal glutamatergic inputs to fast-spiking interneurons.Altered behavioral responses to gamma-aminobutyric acid pharmacological agents in a mouse model of Huntington's disease.Parvalbumin Interneurons Modulate Striatal Output and Enhance Performance during Associative Learning.Progress in developing transgenic monkey model for Huntington's disease.Glial GABA, synthesized by monoamine oxidase B, mediates tonic inhibition.Disrupted striatal neuron inputs and outputs in Huntington's disease.Striatal Direct and Indirect Pathway Output Structures are Differentially Altered in Mouse Models of Huntington's Disease.The adjustment of γ-aminobutyric acidA tonic subunits in Huntington's disease: from transcription to translation to synaptic levels into the neostriatum.Differential changes to D1 and D2 medium spiny neurons in the 12-month-old Q175+/- mouse model of Huntington's Disease
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P2860
Multiple sources of striatal inhibition are differentially affected in Huntington's disease mouse models.
description
2013 nî lūn-bûn
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2013年の論文
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2013年論文
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2013年論文
@zh-hant
2013年論文
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2013年論文
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2013年論文
@zh-tw
2013年论文
@wuu
2013年论文
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2013年论文
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name
Multiple sources of striatal i ...... ington's disease mouse models.
@en
type
label
Multiple sources of striatal i ...... ington's disease mouse models.
@en
prefLabel
Multiple sources of striatal i ...... ington's disease mouse models.
@en
P2093
P2860
P1476
Multiple sources of striatal i ...... ington's disease mouse models.
@en
P2093
Carlos Cepeda
Elian P Botelho
Jane Y Chen
Joseph B Watson
Michael S Levine
Sandra M Holley
Shilpa P Rao
Véronique M André
P2860
P304
P356
10.1523/JNEUROSCI.2137-12.2013
P407
P577
2013-04-01T00:00:00Z