Learning and Memory During Sleep and Anesthesia

Reasor, Jonathan; Poe, Gina R.

doi:10.1097/aia.0b013e318181e513

Cited by 7 publications

(5 citation statements)

References 94 publications

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“…1 Memory is the capacity to retain and revive impressions or to recall or recognize experiences. 2 Memory has been characterized as having three distinct temporal stages: encoding, consolidation, and retrieval.…”

Section: Learning and Memorymentioning

confidence: 99%

Inhibition de l’apprentissage et de la mémoire par les anesthésiques généraux

Wang

Orser

2010

Can J Anesth/J Can Anesth

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Section: Learning and Memorymentioning

confidence: 99%

Inhibition de l’apprentissage et de la mémoire par les anesthésiques généraux

Wang

Orser

2010

Can J Anesth/J Can Anesth

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“…They play critical roles in synaptic plasticity and memory function 7,8. Dysfunction of NMDA receptors has been linked to excitotoxity and neurological disorders, such as epilepsy, schizophrenia, Parkinson's and Huntington's diseases 9.…”

Section: Introductionmentioning

confidence: 99%

“…Biological functions of NMDA receptors are far beyond being the molecular targets of xenon. They play critical roles in synaptic plasticity and memory function. , Dysfunction of NMDA receptors has been linked to excitotoxity and neurological disorders, such as epilepsy, schizophrenia, and Parkinson’s and Huntington’s diseases . NMDA receptors are heterotetrameric cation channels, mostly composed by NR1 and NR2 subunits.…”

Section: Introductionmentioning

confidence: 99%

Mechanistic Insights into Xenon Inhibition of NMDA Receptors from MD Simulations

Liu

Tang

2010

J. Phys. Chem. B

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Inhibition of N-methyl-D-aspartate (NMDA) receptors has been viewed as a primary cause of xenon anesthesia, yet the mechanism is unclear. Here, we investigated interactions between xenon and the ligand-binding domain (LBD) of a NMDA receptor and examined xenon-induced structural and dynamical changes that are relevant to functional changes of the NMDA receptor. Several comparative molecular dynamics simulations were performed on two X-ray structures representing the open- and closed-cleft LBD of the NMDA receptor. We identified plausible xenon action sites in the LBD, including those nearby agonist sites, in the hinge region, and at the interface between two subunits. The xenon binding energy varies from −5.3 to −0.7 kcal/mol. Xenon's effect on the NMDA receptor is conformation-dependent and is produced through both competitive and non-competitive mechanisms. Xenon can promote cleft opening in the absence of agonists and consequently stabilizes the closed channel. Xenon can also bind at the interface of two subunits, alter the inter-subunit interaction, and lead to a reduction of the distance between GT-links. This reduction corresponds to a rearrangement of the channel toward a direction of pore size decreasing, implying a closed or desensitized channel. In addition to these non-competitive actions, xenon was found to weaken the glutamate binding, which could lead to low agonist efficacy and appear as competitive inhibition.

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“…The first term is the mutual information between the ensemble of 100 input spike trains (spanning the interval of a single trial from 0 to T; the ensemble of all presynaptic trains is formally denoted by X(T) = {x j (t) = 4) where angular brackets · Y,X denote averaging over all combinations of input and output spike trains. 1 Here, P(Y|X) is the conditional probability density of our stochastic neuron model to generate a specific spike train Y with (one or several) spike times {t f post } during a trial of duration T given 100 known input spike trains X.…”

Section: Objective Functionmentioning

confidence: 99%

“…Furthermore (4) synaptic memories should show a high degree of stability (Fusi, Drew, & Abbott, 2005) and nevertheless remain plastic (Grossberg, 1987). Moreover, experiments suggest that plasticity rules are (5) sensitive to the presynaptic firing rate (Dudek & Bear, 1992), but (6) depend also on the exact timing of the pre-and postsynaptic spikes (Markram et al, 1997, Bi & Poo, 2001.…”

Section: Introductionmentioning

confidence: 99%

Optimality Model of Unsupervised Spike-Timing-Dependent Plasticity: Synaptic Memory and Weight Distribution

et al. 2007

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We studied the hypothesis that synaptic dynamics is controlled by three basic principles: (1) synapses adapt their weights so that neurons can effectively transmit information, (2) homeostatic processes stabilize the mean firing rate of the postsynaptic neuron, and (3) weak synapses adapt more slowly than strong ones, while maintenance of strong synapses is costly. Our results show that a synaptic update rule derived from these principles shares features, with spike-timing-dependent plasticity, is sensitive to correlations in the input and is useful for synaptic memory. Moreover, input selectivity (sharply tuned receptive fields) of postsynaptic neurons develops only if stimuli with strong features are presented. Sharply tuned neurons can coexist with unselective ones, and the distribution of synaptic weights can be unimodal or bimodal. The formulation of synaptic dynamics through an optimality criterion provides a simple graphical argument for the stability of synapses, necessary for synaptic memory.

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Learning and Memory During Sleep and Anesthesia

Cited by 7 publications

References 94 publications

Inhibition de l’apprentissage et de la mémoire par les anesthésiques généraux

Inhibition de l’apprentissage et de la mémoire par les anesthésiques généraux

Mechanistic Insights into Xenon Inhibition of NMDA Receptors from MD Simulations

Optimality Model of Unsupervised Spike-Timing-Dependent Plasticity: Synaptic Memory and Weight Distribution

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