scholarly journals NMDARs, Coincidence Detectors of Astrocytic and Neuronal Activities

2021 ◽  
Vol 22 (14) ◽  
pp. 7258
Author(s):  
Mark W. Sherwood ◽  
Stéphane H. R. Oliet ◽  
Aude Panatier
Keyword(s):  
Synaptic Plasticity ◽  
Glial Cells ◽  
Spatial Arrangement ◽  
Neurotransmitter Receptors ◽  
Incident Detection ◽  
Dynamic Regulation ◽  
Ability To Act ◽  
Membrane Depolarisation ◽  
Synaptic Level

Synaptic plasticity is an extensively studied cellular correlate of learning and memory in which NMDARs play a starring role. One of the most interesting features of NMDARs is their ability to act as a co-incident detector. It is unique amongst neurotransmitter receptors in this respect. Co-incident detection is possible because the opening of NMDARs requires membrane depolarisation and the binding of glutamate. Opening of NMDARs also requires a co-agonist. Although the dynamic regulation of glutamate and membrane depolarization have been well studied in coincident detection, the role of the co-agonist site is unexplored. It turns out that non-neuronal glial cells, astrocytes, regulate co-agonist availability, giving them the ability to influence synaptic plasticity. The unique morphology and spatial arrangement of astrocytes at the synaptic level affords them the capacity to sample and integrate information originating from unrelated synapses, regardless of any pre-synaptic and post-synaptic commonality. As astrocytes are classically considered slow responders, their influence at the synapse is widely recognized as modulatory. The aim herein is to reconsider the potential of astrocytes to participate directly in ongoing synaptic NMDAR activity and co-incident detection.

scholarly journals The role of glial cells in synaptic function

1999 ◽  
Vol 354 (1381) ◽  
pp. 403-409 ◽  
Author(s):  
Alberto Bacci ◽  
Claudia Verderio ◽  
Elena Pravettoni ◽  
Michela Matteoli
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Synaptic Plasticity ◽  
Cell Population ◽  
Glial Cells ◽  
Synaptic Function ◽  
Synaptic Contacts ◽  
The Central Nervous System ◽  
Active Interaction

Glial cells represent the most abundant cell population in the central nervous system and for years they have been thought to provide just structural and trophic support to neurons. Recently, several studies were performed, leading to the identification of an active interaction between glia and neurons. This paper focuses on the role played by glial cells at the level of the synapse, reviewing recent data defining how glia is determinant in synaptogenesis, in the modulation of fully working synaptic contacts and in synaptic plasticity.

Is astrocyte calcium signaling relevant for synaptic plasticity?

2010 ◽  
Vol 6 (3) ◽  
pp. 147-155 ◽  
Author(s):  
Sarrah Ben Achour ◽  
Lorena Pont-Lezica ◽  
Catherine Béchade ◽  
Olivier Pascual
Keyword(s):  
Synaptic Plasticity ◽  
Calcium Signaling ◽  
Glial Cells ◽  
Direct Interaction ◽  
Cell Types ◽  
Pivotal Role ◽  
Calcium Flux ◽  
Calcium Dependent ◽  
Structural Functions

Astrocytes constitute a major group of glial cells which were long regarded as passive elements, fulfilling nutritive and structural functions for neurons. Calcium rise in astrocytes propagating to neurons was the first demonstration of direct interaction between the two cell types. Since then, calcium has been widely used, not only as an indicator of astrocytic activity but also as a stimulator switch to control astrocyte physiology. As a result, astrocytes have been elevated from auxiliaries to neurons, to cells involved in processing synaptic information. Curiously, while there is evidence that astrocytes play an important role in synaptic plasticity, the data relating to calcium's pivotal role are inconsistent. In this review, we will detail the various mechanisms of calcium flux in astrocytes, then briefly present the calcium-dependent mechanisms of gliotransmitter release. Finally, we will discuss the role of calcium in plasticity and present alternative explanations that could reconcile the conflicting results published recently.

Characteristics Of The Structure Formation Of Gypsum Binder Modified With Zinc Hydrosilicates

2020 ◽  
pp. 40-46
Keyword(s):  
Synergistic Effect ◽  
Physicochemical Properties ◽  
Structure Formation ◽  
Silicic Acid ◽  
Chemical Properties ◽  
Crystal Formation ◽  
Ability To Act ◽  
Chemical Factors ◽  
Sorption Characteristics

The authors' methodic for assessing the role of chemical and physic-chemical factors during the structure formation of gypsum stone is presented in the article. The methodic is also makes it possible to reveal the synergistic effect and to determine the ranges of variation of controls factors that ensure maximum values of such effect. The effect of a micro-sized modifier based on zinc hydro-silicates on the structure formation of building gypsum is analyzed and corresponding dependencies are found. It is shown that effects of influence of modifier on the properties of gypsum compositions are determined by chemical properties of modifier. Among the mentioned properties are sorption characteristics (which depend on the amount of silicic acid and its state) and physicochemical properties - the ability to act as a substrate during crystal formation. The proposed method can also be extended to other binding substances and materials. This article contributes to the understanding of the processes that occur during the structure formation of composites, which will make it possible to control the structure formation in the future, obtaining materials with a given set of properties.

Role of Nicotinic and Muscarinic Receptors on Synaptic Plasticity and Neurological Diseases

2016 ◽  
Vol 22 (14) ◽  
pp. 2004-2014 ◽  
Author(s):  
Marco Fuenzalida ◽  
Miguel Ángel Pérez ◽  
Hugo R. Arias
Keyword(s):  
Synaptic Plasticity ◽  
Muscarinic Receptors ◽  
Neurological Diseases

Pathogenesis of Age-related Cataract: a systematic review of proteomic studies

2020 ◽  
Vol 17 ◽  
Author(s):  
Christina Karakosta ◽  
Argyrios Tzamalis ◽  
Michalis Aivaliotis ◽  
Ioannis Tsinopoulos
Keyword(s):  
Systematic Review ◽  
Oxidant Stress ◽  
Critical Role ◽  
Human Lens ◽  
Nuclear Cataract ◽  
Cataract Formation ◽  
Post Translational Modification ◽  
Ability To Act ◽  
Age Related

Background/Objective:: The aim of this systematic review is to identify all the available data on human lens proteomics with a critical role to age-related cataract formation in order to elucidate the physiopathology of the aging lens. Materials and Methods:: We searched on Medline and Cochrane databases. The search generated 328 manuscripts. We included nine original proteomic studies that investigated human cataractous lenses. Results:: Deamidation was the major age-related post-translational modification. There was a significant increase in the amount of αA-crystallin D-isoAsp58 present at all ages, while an increase in the extent of Trp oxidation was apparent in cataract lenses when compared to aged normal lenses. During aging, enzymes with oxidized cysteine at critical sites included GAPDH, glutathione synthase, aldehyde dehydrogenase, sorbitol dehydrogenase, and PARK7. Conclusion:: D-isoAsp in αA crystallin could be associated with the development of age-related cataract in human, by contributing to the denaturation of a crystallin, and decreasing its ability to act as a chaperone. Oxidation of Trp may be associated with nuclear cataract formation in human, while the role of oxidant stress in age-related cataract formation is dominant.

scholarly journals Dysregulation of Astrocyte–Neuronal Communication in Alzheimer’s Disease

2021 ◽  
Vol 22 (15) ◽  
pp. 7887
Author(s):  
Carmen Nanclares ◽  
Andres Mateo Baraibar ◽  
Alfonso Araque ◽  
Paulo Kofuji
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Synaptic Plasticity ◽  
Neuronal Excitability ◽  
Active Role ◽  
Ionic Homeostasis ◽  
Neuronal Communication ◽  
Structural Support

Recent studies implicate astrocytes in Alzheimer’s disease (AD); however, their role in pathogenesis is poorly understood. Astrocytes have well-established functions in supportive functions such as extracellular ionic homeostasis, structural support, and neurovascular coupling. However, emerging research on astrocytic function in the healthy brain also indicates their role in regulating synaptic plasticity and neuronal excitability via the release of neuroactive substances named gliotransmitters. Here, we review how this “active” role of astrocytes at synapses could contribute to synaptic and neuronal network dysfunction and cognitive impairment in AD.

scholarly journals On the Role of Glial Cells in the Mammalian Nervous System

1974 ◽  
Vol 249 (6) ◽  
pp. 1769-1780
Author(s):  
Bruce K. Schrier ◽  
Edward J. Thompson
Keyword(s):  
Nervous System ◽  
Glial Cells

scholarly journals Monitoring and Modulating Inflammation-Associated Alterations in Synaptic Plasticity: Role of Brain Stimulation and the Blood–Brain Interface

Biomolecules ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 359
Author(s):  
Maximilian Lenz ◽  
Amelie Eichler ◽  
Andreas Vlachos
Keyword(s):  
Synaptic Plasticity ◽  
Brain Stimulation ◽  
Vascular Function ◽  
Neuropsychiatric Symptoms ◽  
Systemic Infection ◽  
Brain Functions ◽  
Blood Brain ◽  
Brain Interface ◽  
The Central Nervous System

Inflammation of the central nervous system can be triggered by endogenous and exogenous stimuli such as local or systemic infection, trauma, and stroke. In addition to neurodegeneration and cell death, alterations in physiological brain functions are often associated with neuroinflammation. Robust experimental evidence has demonstrated that inflammatory cytokines affect the ability of neurons to express plasticity. It has been well-established that inflammation-associated alterations in synaptic plasticity contribute to the development of neuropsychiatric symptoms. Nevertheless, diagnostic approaches and interventional strategies to restore inflammatory deficits in synaptic plasticity are limited. Here, we review recent findings on inflammation-associated alterations in synaptic plasticity and the potential role of the blood–brain interface, i.e., the blood–brain barrier, in modulating synaptic plasticity. Based on recent findings indicating that brain stimulation promotes plasticity and modulates vascular function, we argue that clinically employed non-invasive brain stimulation techniques, such as transcranial magnetic stimulation, could be used for monitoring and modulating inflammation-induced alterations in synaptic plasticity.

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