Dysfunctional cerebellar Purkinje cells contribute to autism-like behaviour in Shank2-deficient mice.
about
Modulation, Plasticity and Pathophysiology of the Parallel Fiber-Purkinje Cell Synapse.SHANK proteins: roles at the synapse and in autism spectrum disorder.Motor Learning Requires Purkinje Cell Synaptic Potentiation through Activation of AMPA-Receptor Subunit GluA3.Cellular and Circuitry Bases of Autism: Lessons Learned from the Temporospatial Manipulation of Autism Genes in the Brain.Cerebellar and Striatal Pathologies in Mouse Models of Autism Spectrum Disorder.Mechanisms underlying vestibulo-cerebellar motor learning in mice depend on movement direction.Secretin Modulates the Postnatal Development of Mouse Cerebellar Cortex Via PKA- and ERK-dependent Pathways.Altered cerebellar connectivity in autism and cerebellar-mediated rescue of autism-related behaviors in mice.Deficiency of Shank2 causes mania-like behavior that responds to mood stabilizers.Expression of mutant DISC1 in Purkinje cells increases their spontaneous activity and impairs cognitive and social behaviors in mice.Maturation, Refinement, and Serotonergic Modulation of Cerebellar Cortical Circuits in Normal Development and in Murine Models of Autism.Impact of NMDA Receptor Overexpression on Cerebellar Purkinje Cell Activity and Motor Learning.Differentiating Cerebellar Impact on Thalamic Nuclei.Chloride Homeostasis in Neurons With Special Emphasis on the Olivocerebellar System: Differential Roles for Transporters and Channels.Heterogeneity of Cell Surface Glutamate and GABA Receptor Expression in Shank and CNTN4 Autism Mouse Models.Shank2 Deletion in Parvalbumin Neurons Leads to Moderate Hyperactivity, Enhanced Self-Grooming and Suppressed Seizure Susceptibility in Mice.Defective Synapse Maturation and Enhanced Synaptic Plasticity in Shank2 Δex7–/– Mice.Distinct Phenotypes of Mouse Models Reflect Neuropsychiatric Spectrum Disorders of Human Patients With VariantsMutant Mice Display Hyperactivity Insensitive to Methylphenidate and Reduced Flexibility in Social Motivation, but Normal Social RecognitionNormal cognitive and social development require posterior cerebellar activityNeonatal brain injury causes cerebellar learning deficits and Purkinje cell dysfunction
P2860
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P2860
Dysfunctional cerebellar Purkinje cells contribute to autism-like behaviour in Shank2-deficient mice.
description
2016 nî lūn-bûn
@nan
2016 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած
@hyw
2016 թվականի սեպտեմբերին հրատարակված գիտական հոդված
@hy
2016年の論文
@ja
2016年論文
@yue
2016年論文
@zh-hant
2016年論文
@zh-hk
2016年論文
@zh-mo
2016年論文
@zh-tw
2016年论文
@wuu
name
Dysfunctional cerebellar Purki ...... viour in Shank2-deficient mice
@nl
Dysfunctional cerebellar Purki ...... iour in Shank2-deficient mice.
@ast
Dysfunctional cerebellar Purki ...... iour in Shank2-deficient mice.
@en
type
label
Dysfunctional cerebellar Purki ...... viour in Shank2-deficient mice
@nl
Dysfunctional cerebellar Purki ...... iour in Shank2-deficient mice.
@ast
Dysfunctional cerebellar Purki ...... iour in Shank2-deficient mice.
@en
prefLabel
Dysfunctional cerebellar Purki ...... viour in Shank2-deficient mice
@nl
Dysfunctional cerebellar Purki ...... iour in Shank2-deficient mice.
@ast
Dysfunctional cerebellar Purki ...... iour in Shank2-deficient mice.
@en
P2093
P2860
P50
P921
P3181
P356
P1476
Dysfunctional cerebellar Purki ...... viour in Shank2-deficient mice
@en
P2093
Chris I De Zeeuw
Claudia M Reinelt
Freek E Hoebeek
Haibo Zhou
Henk-Jan Boele
Jeffrey Stedehouder
Kuikui Zhou
Martijn Schonewille
Michael J Schmeisser
P2860
P2888
P3181
P356
10.1038/NCOMMS12627
P407
P577
2016-09-01T00:00:00Z
P6179
1032390825