G protein-activated inwardly rectifying potassium channels mediate depotentiation of long-term potentiation.
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Pathways and mechanisms of endocytic recyclingBehavioral and Genetic Evidence for GIRK Channels in the CNS: Role in Physiology, Pathophysiology, and Drug AddictionGNB5 mutation causes a novel neuropsychiatric disorder featuring attention deficit hyperactivity disorder, severely impaired language development and normal cognitionGIRK2 splice variants and neuronal G protein-gated K+ channels: implications for channel function and behaviorPyramidal cell selective ablation of N-methyl-D-aspartate receptor 1 causes increase in cellular and network excitability.Reversible plasticity of fear memory-encoding amygdala synaptic circuits even after fear memory consolidation.Effects of individual segmental trisomies of human chromosome 21 syntenic regions on hippocampal long-term potentiation and cognitive behaviors in mice.Dendritic ion channel trafficking and plasticity.Dysfunctional hippocampal inhibition in the Ts65Dn mouse model of Down syndrome.NMDA receptor-dependent GABAB receptor internalization via CaMKII phosphorylation of serine 867 in GABAB1.Hippocampal short- and long-term plasticity are not modulated by astrocyte Ca2+ signaling.The h current is a candidate mechanism for regulating the sliding modification threshold in a BCM-like synaptic learning rule.Emerging roles for G protein-gated inwardly rectifying potassium (GIRK) channels in health and disease.Association study of the KCNJ3 gene as a susceptibility candidate for schizophrenia in the Chinese population.Trisomy of the G protein-coupled K+ channel gene, Kcnj6, affects reward mechanisms, cognitive functions, and synaptic plasticity in mice.GABA and Endocannabinoids Mediate Depotentiation of Schaffer Collateral Synapses Induced by Stimulation of Temperoammonic Inputs.Molecular mechanisms involved in depotentiation and their relevance to schizophrenia.Overexpression of KCNJ3 gene splice variants affects vital parameters of the malignant breast cancer cell line MCF-7 in an opposing manner.A Quantitative Model of the GIRK1/2 Channel Reveals That Its Basal and Evoked Activities Are Controlled by Unequal Stoichiometry of Gα and Gβγ.Increased neuronal activity fragments the Golgi complex.Dual regulation of G proteins and the G-protein-activated K+ channels by lithiumFiring modes of dopamine neurons drive bidirectional GIRK channel plasticity.Tuning and fine-tuning of synapses with adenosine.RGS7/Gβ5/R7BP complex regulates synaptic plasticity and memory by modulating hippocampal GABABR-GIRK signaling.Homeostatic regulation of neuronal excitability by K(+) channels in normal and diseased brains.New insights into the therapeutic potential of Girk channels.G Protein-Gated K+ Channel Ablation in Forebrain Pyramidal Neurons Selectively Impairs Fear Learning.G Protein-Gated Potassium Channels: A Link to Drug Addiction.A KCNJ6 gene polymorphism modulates theta oscillations during reward processing.How does adenosine control neuronal dysfunction and neurodegeneration?mTOR referees memory and disease through mRNA repression and competition.Gbeta5 recruits R7 RGS proteins to GIRK channels to regulate the timing of neuronal inhibitory signaling.G-Protein-Coupled Inwardly Rectifying Potassium (GIRK) Channel Activation by the p75 Neurotrophin Receptor Is Required for Amyloid β Toxicity.Molecular basis of the facilitation of the heterooligomeric GIRK1/GIRK4 complex by cAMP dependent protein kinase.Prolonged seizure activity causes caspase dependent cleavage and dysfunction of G-protein activated inwardly rectifying potassium channelsCannabinoids in Parkinson's DiseaseRecruitment of Gβγ controls the basal activity of G-protein coupled inwardly rectifying potassium (GIRK) channels: crucial role of distal C terminus of GIRK1.Collision coupling in the GABAB receptor-G protein-GIRK signaling cascade.Lithium reduces the span of G protein-activated K(+) (GIRK) channel inhibition in hippocampal neurons.Constructing a road map from synapses to behaviour. Meeting on Synapses: From Molecules to Circuits & Behavior.
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G protein-activated inwardly rectifying potassium channels mediate depotentiation of long-term potentiation.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on 31 December 2008
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
@cs
name
G protein-activated inwardly r ...... ion of long-term potentiation.
@en
G protein-activated inwardly r ...... ion of long-term potentiation.
@nl
type
label
G protein-activated inwardly r ...... ion of long-term potentiation.
@en
G protein-activated inwardly r ...... ion of long-term potentiation.
@nl
prefLabel
G protein-activated inwardly r ...... ion of long-term potentiation.
@en
G protein-activated inwardly r ...... ion of long-term potentiation.
@nl
P2093
P2860
P356
P1476
G protein-activated inwardly r ...... tion of long-term potentiation
@en
P2093
Lily Yeh Jan
Ofer Wiser
Woo-Ping Ge
Xiang Qian
Yuh Nung Jan
P2860
P304
P356
10.1073/PNAS.0811685106
P407
P577
2008-12-31T00:00:00Z