Weakening synapses to cull memories.

Science

Langone Medical Center, New York University, New York, NY, USA.

Published: January 2019

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6552659PMC
http://dx.doi.org/10.1126/science.aaw1675DOI Listing

Publication Analysis

Top Keywords

weakening synapses
4
synapses cull
4
cull memories
4
weakening
1
cull
1
memories
1

Similar Publications

Adaptive remodeling of rat adrenomedullary stimulus-secretion coupling in a chronic hypertensive environment.

Cell Mol Life Sci

December 2024

Univ Angers, INSERM, CNRS, MITOVASC, Équipe CARME, SFR ICAT, F-49000 Angers, France.

Chronic elevated blood pressure impinges on the functioning of multiple organs and therefore harms body homeostasis. Elucidating the protective mechanisms whereby the organism copes with sustained or repetitive blood pressure rises is therefore a topical challenge. Here we address this issue in the adrenal medulla, the master neuroendocrine tissue involved in the secretion of catecholamines, influential hormones in blood pressure regulation.

View Article and Find Full Text PDF

Release your inhibitions: The cell biology of GABAergic postsynaptic plasticity.

Curr Opin Neurobiol

December 2024

Department of Pharmacology, University of Colorado School of Medicine, Anschutz Medical Campus, 12800 East 19th Avenue, Aurora, CO 80045, USA. Electronic address:

GABAergic synaptic inhibition controls circuit function by regulating neuronal plasticity, excitability, and firing. To achieve these goals, inhibitory synapses themselves undergo several forms of plasticity via diverse mechanisms, strengthening and weakening phasic inhibition in response to numerous activity-induced stimuli. These mechanisms include changing the number and arrangement of functional GABARs within the inhibitory postsynaptic domain (iPSD), which can profoundly regulate inhibitory synapse strength.

View Article and Find Full Text PDF

Two types of neuron models are constructed in this paper, namely the single discrete memristive synaptic neuron model and the dual discrete memristive synaptic neuron model. Firstly, it is proved that both models have only one unstable equilibrium point. Then, the influence of the coupling strength parameters and neural membrane amplification coefficient of the corresponding system of the two models on the rich dynamical behavior of the systems is analyzed.

View Article and Find Full Text PDF

Microglial CD2AP deficiency exerts protection in an Alzheimer's disease model of amyloidosis.

Mol Neurodegener

December 2024

Xiamen Key Laboratory of Brain Center, The First Affiliated Hospital of Xiamen University, and Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University, Xiamen, Fujian, 361102, China.

Background: The CD2-associated protein (CD2AP) was initially identified in peripheral immune cells and regulates cytoskeleton and protein trafficking. Single nucleotide polymorphisms (SNPs) in the CD2AP gene have been associated with Alzheimer's disease (AD). However, the functional role of CD2AP, especially its role in microglia during AD onset, remains elusive.

View Article and Find Full Text PDF

Giant miniature endplate potentials at vertebrate neuromuscular junctions: A review.

Eur J Neurosci

December 2024

Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, Texas, USA.

An unusually large amplitude spontaneous miniature endplate potentials (gMEPPs) occur naturally at low frequency at the vertebrate neuromuscular junction. Unlike the normal miniature endplate potentials (nMEPPs), these gMEPPs have long duration and long time to peak. More strikingly, gMEPPs seem to be independent of extracellular and intracellular Ca and have a greater temperature sensitivity than nMEPPs.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!