Impaired dendritic expression and plasticity of h-channels in the fmr1(-/y) mouse model of fragile X syndrome.
about
Dysregulation and restoration of translational homeostasis in fragile X syndromeAltered Neuronal and Circuit Excitability in Fragile X Syndrome.Channelopathies and dendritic dysfunction in fragile X syndrome.Cortical HCN channels: function, trafficking and plasticityThe sodium-activated potassium channel Slack is required for optimal cognitive flexibility in miceIon channels in genetic and acquired forms of epilepsy.From FMRP function to potential therapies for fragile X syndrome.Strings on a Violin: Location Dependence of Frequency Tuning in Active Dendrites5-HT7 receptors as modulators of neuronal excitability, synaptic transmission and plasticity: physiological role and possible implications in autism spectrum disorders.Tonic 5nM DA stabilizes neuronal output by enabling bidirectional activity-dependent regulation of the hyperpolarization activated current via PKA and calcineurin.HCN channels enhance spike phase coherence and regulate the phase of spikes and LFPs in the theta-frequency range.Fmr1 deficiency promotes age-dependent alterations in the cortical synaptic proteome.Short- and long-term plasticity in CA1 neurons from mice lacking h-channel auxiliary subunit TRIP8b.Loss of functional A-type potassium channels in the dendrites of CA1 pyramidal neurons from a mouse model of fragile X syndrome.Age-Dependent Long-Term Potentiation Deficits in the Prefrontal Cortex of the Fmr1 Knockout Mouse Model of Fragile X Syndrome.Increased Persistent Sodium Current Causes Neuronal Hyperexcitability in the Entorhinal Cortex of Fmr1 Knockout Mice.HCN channels are a novel therapeutic target for cognitive dysfunction in Neurofibromatosis type 1.Cell-Type Specific Channelopathies in the Prefrontal Cortex of the fmr1-/y Mouse Model of Fragile X Syndrome.Excitability is increased in hippocampal CA1 pyramidal cells of Fmr1 knockout mice.Identifying specific prefrontal neurons that contribute to autism-associated abnormalities in physiology and social behavior.Delayed in vitro development of Up states but normal network plasticity in Fragile X circuits.High-conductance states and A-type K+ channels are potential regulators of the conductance-current balance triggered by HCN channels.Increased transient Na+ conductance and action potential output in layer 2/3 prefrontal cortex neurons of the fmr1-/y mouse.Dendritic channelopathies contribute to neocortical and sensory hyperexcitability in Fmr1(-/y) mice.Differential Adulthood Onset mGlu5 Signaling Saves Prefrontal Function in the Fragile X Mouse.Translating genetic and preclinical findings into autism therapies.Genetic upregulation of BK channel activity normalizes multiple synaptic and circuit defects in a mouse model of fragile X syndrome.Of Men and Mice: Modeling the Fragile X Syndrome.Impaired hippocampal representation of place in the Fmr1-knockout mouse model of fragile X syndrome.
P2860
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P2860
Impaired dendritic expression and plasticity of h-channels in the fmr1(-/y) mouse model of fragile X syndrome.
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
2012年论文
@zh
2012年论文
@zh-cn
name
Impaired dendritic expression ...... e model of fragile X syndrome.
@ast
Impaired dendritic expression ...... e model of fragile X syndrome.
@en
type
label
Impaired dendritic expression ...... e model of fragile X syndrome.
@ast
Impaired dendritic expression ...... e model of fragile X syndrome.
@en
prefLabel
Impaired dendritic expression ...... e model of fragile X syndrome.
@ast
Impaired dendritic expression ...... e model of fragile X syndrome.
@en
P2860
P1433
P1476
Impaired dendritic expression ...... se model of fragile X syndrome
@en
P2093
Arvin R Akhavan
Daniel Johnston
P2860
P304
P356
10.1016/J.CELREP.2012.02.002
P577
2012-03-01T00:00:00Z