scholarly journals Editorial: Neuronal Pathways Affecting Glial Function

2021 ◽  
Vol 15 ◽  
Author(s):  
Yossi Buskila ◽  
Erika Gyengési ◽  
John W. Morley
Keyword(s):  
Glial Function

scholarly journals Neurons and Glia Interplay in α-Synucleinopathies

2021 ◽  
Vol 22 (9) ◽  
pp. 4994
Author(s):  
Panagiota Mavroeidi ◽  
Maria Xilouri
Keyword(s):  
Glial Cells ◽  
Current Knowledge ◽  
Lewy Bodies ◽  
Alpha Synuclein ◽  
Lewy Neurites ◽  
Cytoplasmic Inclusions ◽  
Glial Cytoplasmic Inclusions ◽  
Glial Function ◽  
Presynaptic Protein

Accumulation of the neuronal presynaptic protein alpha-synuclein within proteinaceous inclusions represents the key histophathological hallmark of a spectrum of neurodegenerative disorders, referred to by the umbrella term a-synucleinopathies. Even though alpha-synuclein is expressed predominantly in neurons, pathological aggregates of the protein are also found in the glial cells of the brain. In Parkinson’s disease and dementia with Lewy bodies, alpha-synuclein accumulates mainly in neurons forming the Lewy bodies and Lewy neurites, whereas in multiple system atrophy, the protein aggregates mostly in the glial cytoplasmic inclusions within oligodendrocytes. In addition, astrogliosis and microgliosis are found in the synucleinopathy brains, whereas both astrocytes and microglia internalize alpha-synuclein and contribute to the spread of pathology. The mechanisms underlying the pathological accumulation of alpha-synuclein in glial cells that under physiological conditions express low to non-detectable levels of the protein are an area of intense research. Undoubtedly, the presence of aggregated alpha-synuclein can disrupt glial function in general and can contribute to neurodegeneration through numerous pathways. Herein, we summarize the current knowledge on the role of alpha-synuclein in both neurons and glia, highlighting the contribution of the neuron-glia connectome in the disease initiation and progression, which may represent potential therapeutic target for a-synucleinopathies.

scholarly journals Assessment of Glial Function in the In Vivo Retina

2011 ◽  
pp. 499-514 ◽  
Author(s):  
Anja I. Srienc ◽  
Tess E. Kornfield ◽  
Anusha Mishra ◽  
Michael A. Burian ◽  
Eric A. Newman
Keyword(s):  
Glial Function

Glial Function in Homeostasis of the Neuronal Microenvironment

Physiology ◽  
1994 ◽  
Vol 9 (6) ◽  
pp. 265-267
Author(s):  
RK Orkand ◽  
SC Opava
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Small Molecules ◽  
Transport Systems ◽  
Large Area ◽  
Glial Function ◽  
The Central Nervous System ◽  
Glial Membrane ◽  
Membrane Transport Systems ◽  
Specific Membrane

Neuroglia buffer changes in the concentrations of ions and small molecules in the tortuous network of narrow extracellular clefts that constitutes the functional environment of neurons in the central nervous system. The large area of glial membrane bordering this space exhibits specific membrane transport systems for homeostasis.

scholarly journals Glial pathology in neuropsychiatric disorders: a brief review

2019 ◽  
Vol 30 (4) ◽  
Author(s):  
Shilpa Borehalli Mayegowda ◽  
Christofer Thomas
Keyword(s):  
Nervous System ◽  
Prefrontal Cortex ◽  
Glial Cells ◽  
Cell Function ◽  
Neuropsychiatric Disorders ◽  
Brain Regions ◽  
Neuronal Function ◽  
Glial Function ◽  
Clinical Conditions ◽  
Stress Models

Abstract Neurons have been considered the major functional entities of the nervous system that are responsible for most of the functions even though glial cells largely outnumber them. However, recent reports have proved that glial cells do not function just like glue in the nervous system but also substantially affect neuronal function and activities, and are significantly involved in the underlying pathobiology of various psychiatric disorders. Dysfunctional astrocytes and degeneration of glial cells are postulated to be critical factors contributing to the aggravation of depressive-like symptoms in humans, which was proved using animal models. Alteration in glial cell function predominantly targets three main brain regions – the prefrontal cortex, limbic areas including the hippocampus, and the amygdala, which have been extensively studied by various researchers across the globe. These studies have postulated that failure in adopting to the changing neurophysiology due to stress will lead to regressive plasticity in the hippocampus and prefrontal cortex, but to progressive plasticity in the amygdala. In this present review, an effort has been made to understand the different alterations in chronic stress models in correlation with clinical conditions, providing evidence on the defective maintenance of glial function and its potential role in the precipitation of neuropsychiatric disorders.

scholarly journals Chronic Stress and Glucocorticoids: From Neuronal Plasticity to Neurodegeneration

2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Sheela Vyas ◽  
Ana João Rodrigues ◽  
Joana Margarida Silva ◽  
Francois Tronche ◽  
Osborne F. X. Almeida ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Prolonged Exposure ◽  
Stress Hormones ◽  
Behavioral Adaptation ◽  
Mineralocorticoid Receptors ◽  
Cellular Mechanisms ◽  
Ample Evidence ◽  
Synaptic Structure ◽  
Glial Function ◽  
Prolonged Stress

Stress and stress hormones, glucocorticoids (GCs), exert widespread actions in central nervous system, ranging from the regulation of gene transcription, cellular signaling, modulation of synaptic structure, and transmission and glial function to behavior. Their actions are mediated by glucocorticoid and mineralocorticoid receptors which are nuclear receptors/transcription factors. While GCs primarily act to maintain homeostasis by inducing physiological and behavioral adaptation, prolonged exposure to stress and elevated GC levels may result in neuro- and psychopathology. There is now ample evidence for cause-effect relationships between prolonged stress, elevated GC levels, and cognitive and mood disorders while the evidence for a link between chronic stress/GC and neurodegenerative disorders such as Alzheimer’s (AD) and Parkinson’s (PD) diseases is growing. This brief review considers some of the cellular mechanisms through which stress and GC may contribute to the pathogenesis of AD and PD.

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