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Selective impairment of learning and blockade of long-term potentiation by an N-methyl-D-aspartate receptor antagonist, AP5
TLDR
It is reported that chronic intraventricular infusion of D, L-AP5 causes a selective impairment of place learning, which is highly sensitive to hippocampal damage7, without affecting visual discrimination learning,which is not8 and suggest that NMDA receptors are involved in spatial learning, and add support to the hypothesis that LTP is involved in some, but not all, forms of learning. Expand
A Glycine Site Associated with N‐Methyl‐d‐Aspartic Acid Receptors: Characterization and Identification of a New Class of Antagonists
TLDR
Kynurenate‐type compounds inhibit glycine binding and are suggested to form a novel class of antagonists of the NMDA receptor acting through the glycine site, suggesting the existence of a dual and opposite modulation of NMDA receptors by endogenous ligands. Expand
Progesterone receptors: Form and function in brain
TLDR
The impact of clinically used progestogens and developing selective PR modulators for targeted outcomes in brain is a critical avenue of investigation as the non-reproductive functions of PRs have far-reaching implications for hormone therapy to maintain neurological health and function throughout menopausal aging. Expand
The tyrosine kinase and mitogen-activated protein kinase pathways mediate multiple effects of estrogen in hippocampus.
TLDR
Estrogen replacement therapy in women is associated with improvement of cognitive deficits and reduced incidence of Alzheimer's disease, and estrogen is neuroprotective against N-methyl-d-aspartate- and kainate-mediated neurotoxicity, an effect mediated by tyrosine kinase/mitogen-activated protein kinase (MAPK) pathways. Expand
Developmental Changes in NMDA Neurotoxicity Reflect Developmental Changes in Subunit Composition of NMDA Receptors
TLDR
The results are consistent with the idea that NMDA-mediated toxicity is caused by activation of NR2B- but not NR2A-containing NMDA receptors leading to calpain activation and that developmental changes in NMDA toxicity reflect developmental changesIn NMDA receptor subunit composition. Expand
The biochemistry of memory: a new and specific hypothesis.
TLDR
A synaptic process with properties required for an intermediate step in memory storage is uncovered and hypothesized to be responsible for those forms of memory localized in the telencephalon. Expand
SIRT1 Is Essential for Normal Cognitive Function and Synaptic Plasticity
TLDR
It is shown that SIRT1 is expressed in neurons of the hippocampus, a key structure in learning and memory and indispensable for normal learning, memory, and synaptic plasticity in mice. Expand
SIRT1 is essential for normal cognitive function and synaptic plasticity.
Conservation of normal cognitive functions relies on the proper performance of the nervous system at the cellular and molecular level. The mammalian nicotinamide-adenine dinucleotide-dependentExpand
Cyclic changes in estradiol regulate synaptic plasticity through the MAP kinase pathway
TLDR
It is reported that endogenous estrogen produces a tonic phosphorylation/activation of extracellular signal-regulated kinase 2 (ERK2)/MAP kinase throughout the female rat brain and an increase in tyrosineosphorylation of NR2 subunits of N-methyl-d-aspartate (NMDA) receptors. Expand
Synaptotagmin IV is an immediate early gene induced by depolarization in PC12 cells and in brain.
TLDR
The SytIV gene may provide a direct link between depolarization-induced neuronal gene expression and subsequent modulation of synaptic structure and function. Expand
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