Genetic disruption of cortical interneuron development causes region- and GABA cell type-specific deficits, epilepsy, and behavioral dysfunction.
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Convulsing toward the pathophysiology of autismDlx5 and Dlx6 regulate the development of parvalbumin-expressing cortical interneurons.The genetic and neurobiologic compass points toward common signaling dysfunctions in autism spectrum disordersA genetic variant that disrupts MET transcription is associated with autismCommon circuit defect of excitatory-inhibitory balance in mouse models of autism.Genes and brain malformations associated with abnormal neuron positioningAnterior Cingulate epilepsy: mechanisms and modulationFgfr1 inactivation in the mouse telencephalon results in impaired maturation of interneurons expressing parvalbuminCortical Neural Computation by Discrete Results HypothesisDecreased Serum Hepatocyte Growth Factor (HGF) in Autistic Children with Severe Gastrointestinal DiseaseThe requirement of Nkx2-1 in the temporal specification of cortical interneuron subtypesPrenatal exposure of ethanol induces increased glutamatergic neuronal differentiation of neural progenitor cellsIncreasing proportions of tyrosine hydroxylase-immunoreactive interneurons colocalize with choline acetyltransferase or vasoactive intestinal peptide in the developing rat cerebral cortexRecent Advances in the Genetics of Vocal LearningA triplet repeat expansion genetic mouse model of infantile spasms syndrome, Arx(GCG)10+7, with interneuronopathy, spasms in infancy, persistent seizures, and adult cognitive and behavioral impairmentAdvanced microscopic imaging methods to investigate cortical development and the etiology of mental retardation.Netrin-1-alpha3beta1 integrin interactions regulate the migration of interneurons through the cortical marginal zone.Decreased number of interneurons and increased seizures in neuropilin 2 deficient mice: implications for autism and epilepsy.Selective cortical interneuron and GABA deficits in cyclin D2-null mice.Genetic evidence implicating multiple genes in the MET receptor tyrosine kinase pathway in autism spectrum disorder.HCN Channel Modulation of Synaptic Integration in GABAergic Interneurons in Malformed Rat Neocortex.Hepatocyte growth factor (HGF) modulates GABAergic inhibition and seizure susceptibility.Association of genetic variation in the MET proto-oncogene with schizophrenia and general cognitive ability.Anxiety, memory impairment, and locomotor dysfunction caused by a mutant thyroid hormone receptor alpha1 can be ameliorated by T3 treatment.Tbr2-positive intermediate (basal) neuronal progenitors safeguard cerebral cortex expansion by controlling amplification of pallial glutamatergic neurons and attraction of subpallial GABAergic interneuronsHaploinsufficiency of the E3 ubiquitin ligase C-terminus of heat shock cognate 70 interacting protein (CHIP) produces specific behavioral impairments.Prenatal polycyclic aromatic hydrocarbon exposure leads to behavioral deficits and downregulation of receptor tyrosine kinase, MET.Urokinase-type plasminogen activator promotes dendritic spine recovery and improves neurological outcome following ischemic strokeAdipokines: a link between obesity and dementia?Altered intrinsic properties of neuronal subtypes in malformed epileptogenic cortex.The promise of an interneuron-based cell therapy for epilepsyUse of "MGE enhancers" for labeling and selection of embryonic stem cell-derived medial ganglionic eminence (MGE) progenitors and neurons.Deletion of Dlx1 results in reduced glutamatergic input to hippocampal interneurons.Predicting novel histopathological microlesions in human epileptic brain through transcriptional clusteringA deficiency of uPAR alters endothelial angiogenic function and cell morphology.Interneurons are necessary for coordinated activity during reversal learning in orbitofrontal cortex.GABAB receptors in maintenance of neocortical circuit function.Reversal learning and attentional set-shifting in mice.A surprising METamorphosis: autism genetics finds a common functional variant.Genetics and function of neocortical GABAergic interneurons in neurodevelopmental disorders
P2860
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P2860
Genetic disruption of cortical interneuron development causes region- and GABA cell type-specific deficits, epilepsy, and behavioral dysfunction.
description
2003 nî lūn-bûn
@nan
2003年の論文
@ja
2003年学术文章
@wuu
2003年学术文章
@zh
2003年学术文章
@zh-cn
2003年学术文章
@zh-hans
2003年学术文章
@zh-my
2003年学术文章
@zh-sg
2003年學術文章
@yue
2003年學術文章
@zh-hant
name
Genetic disruption of cortical ...... y, and behavioral dysfunction.
@en
Genetic disruption of cortical ...... y, and behavioral dysfunction.
@nl
type
label
Genetic disruption of cortical ...... y, and behavioral dysfunction.
@en
Genetic disruption of cortical ...... y, and behavioral dysfunction.
@nl
prefLabel
Genetic disruption of cortical ...... y, and behavioral dysfunction.
@en
Genetic disruption of cortical ...... y, and behavioral dysfunction.
@nl
P2093
P1476
Genetic disruption of cortical ...... sy, and behavioral dysfunction
@en
P2093
Caleb Davis
Daniel B Campbell
Elizabeth M Powell
Gregg D Stanwood
Jeffrey L Noebels
Pat Levitt
P304
P356
10.1523/JNEUROSCI.23-02-00622.2003
P407
P577
2003-01-01T00:00:00Z