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The substrates of memory: defects, treatments, and enhancement.

The substrates of memory: defects, treatments, and enhancement.

http://www.wikidata.org/entity/Q36718516

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Ampakines cause sustained increases in brain-derived neurotrophic factor signaling at excitatory synapses without changes in AMPA receptor subunit expression FK506-binding protein 1b/12.6: a key to aging-related hippocampal Ca2+ dysregulation?AMPAKINE enhancement of social interaction in the BTBR mouse model of autism A BDNF loop-domain mimetic acutely reverses spontaneous apneas and respiratory abnormalities during behavioral arousal in a mouse model of Rett syndrome.Progesterone-estrogen interactions in synaptic plasticity and neuroprotection.Working memory deficits, increased anxiety-like traits, and seizure susceptibility in BDNF overexpressing mice.NGF is essential for hippocampal plasticity and learning.Presynaptic BDNF promotes postsynaptic long-term potentiation in the dorsal striatum BDNF signaling during learning is regionally differentiated within hippocampus Fluctuations in endogenous kynurenic acid control hippocampal glutamate and memory Correlated memory defects and hippocampal dendritic spine loss after acute stress involve corticotropin-releasing hormone signaling.Physiological activation of synaptic Rac>PAK (p-21 activated kinase) signaling is defective in a mouse model of fragile X syndrome.Loss of the fragile X mental retardation protein decouples metabotropic glutamate receptor dependent priming of long-term potentiation from protein synthesis.Acute BDNF treatment upregulates GluR1-SAP97 and GluR2-GRIP1 interactions: implications for sustained AMPA receptor expression.A loss-of-function screen for phosphatases that regulate neurite outgrowth identifies PTPN12 as a negative regulator of TrkB tyrosine phosphorylation.The molecular and cellular biology of enhanced cognition.The likelihood of cognitive enhancement Estrogen promotes learning-related plasticity by modifying the synaptic cytoskeleton.Neurons and networks organizing and sequencing memories.Binding to and Inhibition of Insulin-Regulated Aminopeptidase by Macrocyclic Disulfides Enhances Spine Density.UBE3A Regulates Synaptic Plasticity and Learning and Memory by Controlling SK2 Channel Endocytosis LTP induction translocates cortactin at distant synapses in wild-type but not Fmr1 knock-out mice.A nonlinear model for hippocampal cognitive prosthesis: memory facilitation by hippocampal ensemble stimulation.Fragmentation and unpredictability of early-life experience in mental disorders.BDNF Induces Striatal-Enriched Protein Tyrosine Phosphatase 61 Degradation Through the Proteasome.Potential therapeutic approaches for Angelman syndrome.A TrkB small molecule partial agonist rescues TrkB phosphorylation deficits and improves respiratory function in a mouse model of Rett syndrome Oroxylin A Induces BDNF Expression on Cortical Neurons through Adenosine A2A Receptor Stimulation: A Possible Role in Neuroprotection NMDA receptor activation and calpain contribute to disruption of dendritic spines by the stress neuropeptide CRH.A small molecule TrkB ligand reduces motor impairment and neuropathology in R6/2 and BACHD mouse models of Huntington's disease.Modulation of synaptic transmission and plasticity by cell adhesion and repulsion molecules.Glucocorticoid receptors are localized to dendritic spines and influence local actin signaling.Transcriptional and epigenetic regulation of Hebbian and non-Hebbian plasticity.Forgetting and small G protein Rac.AMPA receptors as drug targets in neurological disease--advantages, caveats, and future outlook.Differences between synaptic plasticity thresholds result in new timing rules for maximizing long-term potentiation.Angelman syndrome: Current and emerging therapies in 2016.Emotional Modulation of Learning and Memory: Pharmacological Implications.AMPA receptor-induced local brain-derived neurotrophic factor signaling mediates motor recovery after stroke Anesthetic Alterations of Collective Terahertz Oscillations in Tubulin Correlate with Clinical Potency: Implications for Anesthetic Action and Post-Operative Cognitive Dysfunction.

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P2860

The substrates of memory: defects, treatments, and enhancement.

http://www.wikidata.org/entity/Q36718516

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2008 nî lūn-bûn

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2008年論文

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The substrates of memory: defects, treatments, and enhancement.

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J.EJPHAR.2007.11.082

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European Journal of Pharmacology

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The substrates of memory: defects, treatments, and enhancement.

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Christine M Gall

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Christopher S Rex

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Gary Lynch

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Lulu Y Chen

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P2860

Rho proteins, mental retardation and the cellular basis of cognition

Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path

Facilitation of glutamate receptors enhances memory

Centrally active modulators of glutamate receptors facilitate the induction of long-term potentiation in vivo

Abnormal dendritic spines in fragile X knockout mice: maturation and pruning deficits

Structural changes at dendritic spine synapses during long-term potentiation

Chronic elevation of brain-derived neurotrophic factor by ampakines

Loss of huntingtin-mediated BDNF gene transcription in Huntington's disease

Selective impairment of learning and blockade of long-term potentiation by an N-methyl-D-aspartate receptor antagonist, AP5

Glutamate-based therapeutic approaches: ampakines

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