NITRIC OXIDE, SYNAPTIC PLASTICITY AND MEMORY FORMATION IN THE BRAIN

1998 ◽  
pp. 151-158
Author(s):  
G. ANDREES BÖHME
Keyword(s):  
Nitric Oxide ◽  
Synaptic Plasticity ◽  
Memory Formation ◽  
The Brain

scholarly journals Modulation of AMPA Receptors by Nitric Oxide in Nerve Cells

2020 ◽  
Vol 21 (3) ◽  
pp. 981 ◽  
Author(s):  
Violetta O. Ivanova ◽  
Pavel M. Balaban ◽  
Natalia V. Bal
Keyword(s):  
Nitric Oxide ◽  
Synaptic Plasticity ◽  
Ampa Receptors ◽  
Surface Expression ◽  
Gaseous Molecule ◽  
Main Target ◽  
Nmda Glutamate Receptors ◽  
Synaptic Changes ◽  
The Brain

Nitric oxide (NO) is a gaseous molecule with a large number of functions in living tissue. In the brain, NO participates in numerous intracellular mechanisms, including synaptic plasticity and cell homeostasis. NO elicits synaptic changes both through various multi-chain cascades and through direct nitrosylation of targeted proteins. Along with the N-methyl-d-aspartate (NMDA) glutamate receptors, one of the key components in synaptic functioning are α-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptors—the main target for long-term modifications of synaptic effectivity. AMPA receptors have been shown to participate in most of the functions important for neuronal activity, including memory formation. Interactions of NO and AMPA receptors were observed in important phenomena, such as glutamatergic excitotoxicity in retinal cells, synaptic plasticity, and neuropathologies. This review focuses on existing findings that concern pathways by which NO interacts with AMPA receptors, influences properties of different subunits of AMPA receptors, and regulates the receptors’ surface expression.

scholarly journals Reading Memory Formation from the Eyes

2018 ◽  
Author(s):  
Anne Bergt ◽  
Anne E. Urai ◽  
Tobias H. Donner ◽  
Lars Schwabe
Keyword(s):  
Synaptic Plasticity ◽  
Memory Formation ◽  
Pupil Dilation ◽  
Long Term Memory ◽  
Term Memory ◽  
Pupil Response ◽  
Rapid Formation ◽  
The Brain

At any time, we are processing thousands of stimuli, but only few of them will be remembered hours or days later. Is there any way to predict which ones? Here, we show that the pupil response to ongoing stimuli, an indicator of physiological arousal, is a reliable predictor of long-term memory for these stimuli, over at least one day. Pupil dilation was tracked while participants performed visual and auditory encoding tasks. Memory was tested immediately after encoding and 24 hours later. Irrespective of the encoding modality, trial-by-trial variations in pupil dilation predicted which stimuli were recalled in the immediate and 24 hours-delayed tests. These results show that our eyes may provide a window into the formation of long-term memories. Furthermore, our findings underline the important role of central arousal systems in the rapid formation of memories in the brain, possibly by gating synaptic plasticity mechanisms.

scholarly journals The synaptic plasticity and memory hypothesis: encoding, storage and persistence

2014 ◽  
Vol 369 (1633) ◽  
pp. 20130288 ◽  
Author(s):  
Tomonori Takeuchi ◽  
Adrian J. Duszkiewicz ◽  
Richard G. M. Morris
Keyword(s):  
Synaptic Plasticity ◽  
Optical Imaging ◽  
Brain Area ◽  
Molecular Genetic ◽  
Memory Formation ◽  
New Work ◽  
Necessary And Sufficient ◽  
Activity Dependent ◽  
The Brain

The synaptic plasticity and memory hypothesis asserts that activity-dependent synaptic plasticity is induced at appropriate synapses during memory formation and is both necessary and sufficient for the encoding and trace storage of the type of memory mediated by the brain area in which it is observed. Criteria for establishing the necessity and sufficiency of such plasticity in mediating trace storage have been identified and are here reviewed in relation to new work using some of the diverse techniques of contemporary neuroscience. Evidence derived using optical imaging, molecular-genetic and optogenetic techniques in conjunction with appropriate behavioural analyses continues to offer support for the idea that changing the strength of connections between neurons is one of the major mechanisms by which engrams are stored in the brain.

scholarly journals Epigenetic Mechanisms in Memory and Cognitive Decline Associated with Aging and Alzheimer’s Disease

2021 ◽  
Vol 22 (22) ◽  
pp. 12280
Author(s):  
Sabyasachi Maity ◽  
Kayla Farrell ◽  
Shaghayegh Navabpour ◽  
Sareesh Naduvil Narayanan ◽  
Timothy J. Jarome
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Synaptic Plasticity ◽  
Memory Loss ◽  
Memory Formation ◽  
Epigenetic Modifications ◽  
Epigenetic Mechanisms ◽  
Post Translational Modifications ◽  
Memory Decline ◽  
The Brain

Epigenetic mechanisms, which include DNA methylation, a variety of post-translational modifications of histone proteins (acetylation, phosphorylation, methylation, ubiquitination, sumoylation, serotonylation, dopaminylation), chromatin remodeling enzymes, and long non-coding RNAs, are robust regulators of activity-dependent changes in gene transcription. In the brain, many of these epigenetic modifications have been widely implicated in synaptic plasticity and memory formation. Dysregulation of epigenetic mechanisms has been reported in the aged brain and is associated with or contributes to memory decline across the lifespan. Furthermore, alterations in the epigenome have been reported in neurodegenerative disorders, including Alzheimer’s disease. Here, we review the diverse types of epigenetic modifications and their role in activity- and learning-dependent synaptic plasticity. We then discuss how these mechanisms become dysregulated across the lifespan and contribute to memory loss with age and in Alzheimer’s disease. Collectively, the evidence reviewed here strongly supports a role for diverse epigenetic mechanisms in memory formation, aging, and neurodegeneration in the brain.

scholarly journals MuSK Expressed in the Brain Mediates Cholinergic Responses, Synaptic Plasticity, and Memory Formation

2006 ◽  
Vol 26 (30) ◽  
pp. 7919-7932 ◽  
Author(s):  
A. Garcia-Osta ◽  
P. Tsokas ◽  
G. Pollonini ◽  
E. M. Landau ◽  
R. Blitzer ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Memory Formation ◽  
The Brain

Localization of the cGMP-dependent protein kinases in relation to nitric oxide synthase in the brain

1999 ◽  
Vol 17 (1) ◽  
pp. 45-55 ◽  
Author(s):  
A.E.-D El-Husseini ◽  
J Williams ◽  
P.B Reiner ◽  
S Pelech ◽  
S.R Vincent
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Protein Kinases ◽  
Dependent Protein ◽  
Oxide Synthase ◽  
The Brain

scholarly journals Genotoxic and oxidative effect of duloxetine on mouse brain and liver tissues

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Isela Álvarez-González ◽  
Scarlett Camacho-Cantera ◽  
Patricia Gómez-González ◽  
Michael J. Rendón Barrón ◽  
José A. Morales-González ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Dna Damage ◽  
Mouse Brain ◽  
Control Level ◽  
Dna Oxidation ◽  
Methyl Methanesulfonate ◽  
Control Group ◽  
Oxidative Potential ◽  
The Brain ◽  
Oxidative Effect

AbstractWe evaluated the duloxetine DNA damaging capacity utilizing the comet assay applied to mouse brain and liver cells, as well as its DNA, lipid, protein, and nitric oxide oxidative potential in the same cells. A kinetic time/dose strategy showed the effect of 2, 20, and 200 mg/kg of the drug administered intraperitoneally once in comparison with a control and a methyl methanesulfonate group. Each parameter was evaluated at 3, 9, 15, and 21 h postadministration in five mice per group, except for the DNA oxidation that was examined only at 9 h postadministration. Results showed a significant DNA damage mainly at 9 h postexposure in both organs. In the brain, with 20 and 200 mg/kg we found 50 and 80% increase over the control group (p ≤ 0.05), in the liver, the increase of 2, 20, and 200 mg/kg of duloxetine was 50, 80, and 135% in comparison with the control level (p ≤ 0.05). DNA, lipid, protein and nitric oxide oxidation increase was also observed in both organs. Our data established the DNA damaging capacity of duloxetine even with a dose from the therapeutic range (2 mg/kg), and suggest that this effect can be related with its oxidative potential.

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