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Journal ArticleDOI

NMDA receptors and memory encoding

Richard G. M. Morris
- 01 Nov 2013 - 
- Vol. 74, pp 32-40
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TLDR
How my then interest in long-term potentiation (LTP) as a model of memory enabled me to recognise the importance of Collingridge et al.'s discovery is laid out - and how the idea that NMDA receptor activation is essential for memory encoding, though not for storage, took time to develop and to be accepted.
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This article is published in Neuropharmacology.The article was published on 2013-11-01. It has received 234 citations till now. The article focuses on the topics: Synaptic plasticity & Long-term potentiation.

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Citations
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Journal ArticleDOI

Time and space profiling of NMDA receptor co-agonist functions.

TL;DR: The most advanced knowledge of how glycine and d‐serine may orchestrate synapse dynamics and drive neuronal network activity in a time‐ and synapse‐specific manner is integrated and how changes in synaptic availability of these amino acids may contribute to cognitive impairments such as those associated with healthy aging, epilepsy, and schizophrenia are integrated.
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Synaptic Plasticity, Metaplasticity and Depression

TL;DR: The growing evidence that long-term synaptic changes in glutamatergic transmission, in brain regions that regulate mood, are key determinants of affective homeostasis and therapeutic targets with immense potential for drug development is reviewed.
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Behavioral neuroscience of psychological pain

TL;DR: This article briefly discusses the daily-life significance of psychological pain and centers on a discussion of the results originating from two procedures involving incentive loss: successive negative contrast-the unexpected devaluation of a reward-and appetitive extinction- the unexpected omission of a Reward.
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Glutamatergic regulation of cognition and functional brain connectivity: insights from pharmacological, genetic and translational schizophrenia research.

TL;DR: It is highlighted how glutamatergic dysfunction, and NMDA receptor hypofunction in particular, is a key mechanism contributing to the cognitive deficits observed in schizophrenia and some of the glutamatorgic targets that have been tested as putative procognitive targets for this disorder are outlined.
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Metabotropic Glutamate Receptors Induce a Form of LTP Controlled by Translation and Arc Signaling in the Hippocampus

TL;DR: It is reported that an NMDAR-independent form of LTP, initially characterized as dependent on voltage-gated Ca2+ channels, also requires the activation of mGluRs, suggesting the coexistence of two distinct activity-dependent systems of bidirectional synaptic plasticity.
References
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Neural networks and physical systems with emergent collective computational abilities

TL;DR: A model of a system having a large number of simple equivalent components, based on aspects of neurobiology but readily adapted to integrated circuits, produces a content-addressable memory which correctly yields an entire memory from any subpart of sufficient size.
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Place navigation impaired in rats with hippocampal lesions.

TL;DR: It is reported that, in addition to a spatial discrimination impairment, total hippocampal lesions also cause a profound and lasting placenavigational impairment that can be dissociated from correlated motor, motivational and reinforcement aspects of the procedure.
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Neural computation of decisions in optimization problems

TL;DR: Results of computer simulations of a network designed to solve a difficult but well-defined optimization problem-the Traveling-Salesman Problem-are presented and used to illustrate the computational power of the networks.
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Magnesium gates glutamate-activated channels in mouse central neurones

TL;DR: The voltage dependence of the NMDA receptor-linked conductance appears to be a consequence of the voltage dependenceof the Mg2+ block and its interpretation does not require the implication of an intramembrane voltage-dependent ‘gate’.
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Selective impairment of learning and blockade of long-term potentiation by an N -methyl-D-aspartate receptor antagonist, AP5

TL;DR: This article showed that chronic intraventricular infusion of D,L-AP5 causes a selective impairment of place learning, which is highly sensitive to hippocampal damage, without affecting visual discrimination learning.
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