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Editorial

Astrocyte, reactive astrocytes and self-regulative

apoptosis in the neuroinflammation

Liang-Wei Chen
Institute of Neurosciences, Department of Neurobiology and Collaborative Innovation Center for Brain Science, The Fourth
Military Medical University, Xi’an 710032, Shaanxi, China.

Astrocyte, one of the most abundant glial cell types, in synaptic transmission is controlled by the astrocytic
actively functions in stabilizing neural circuits and GLT-1, i.e. while impairing GLT-1 diffusion could slow
synaptic transmission in the central nervous system kinetics of excitatory currents or prolonged time course
(CNS). Astrocytes not only provide metabolic and of synaptic glutamate transmission. [5]
trophic supports to various CNS neurons and but
also actively work in assisting synaptic transmission Reactive astrocytes, a most common pathological
and plasticity. A line of growing evidences have hallmark, contribute to pathogenesis or progression
documented that astrocytes present as an essential of neurological disorders like trauma, ischemia,
coordinatorin neural circuit function. Firstly, calcium Alzheimer’s and Parkinson’s disease (PD). Astrocytes
[1]
signaling or calcium wave calcium (Ca ) between can in vitro and in vivo respond to various stimuli in
2+
neighboring astrocytes contribute to establishment of a trauma, ischemia and diseased conditions, fast change
huge astrocytic glial network by gap-junctions, which morphology and functional properties, and many
has updated the understanding of astrocyte function appear asactivated or become reactive astrocytes.
in CNS, and led to an idea that astrocytes are powerful Reactive astrocytes undergo phenotypic changes and
regulators of neuronal spiking, synaptic plasticity and contribute to pathogenesis or progression of neurological
brain blood flow as well. The Ca wave in astrocyte disorders. For instance, those reactive astrocytes
[2]
2+
processes may also precede onset of hyperemia and have been proposed to be incompetent bystanders
in epileptogenesis as a result of cellular changes
function as regulators of neurovascular coupling. rendering them unable to perform housekeeping
[3]
Secondly, astrocytes can also fast respond to sensory functions in diseased CNS. Astrocytes modulate
[6]
stimulation and involve in generation of neuronal excitatory and inhibitory balance by regulating
rhythmic activity, and blockade with a Ca chelator can astrocytic uptake of gamma amino acid butyric acid
2+
sufficiently prevent neurons from a rhythmic bursting, and glutamate efficiency. The reactive astrocytes or
[7]
indicating that astrocytes partially and critically astrogliosis resulting from neuronal hyperexcitability
contribute a fundamental neuronal firingpattern or further render inhibitory activity in epilepsy. New
[4]
generation of rhythmic activity. Thirdly, distinct findings have thus challenged us to consider an
astrocytic transporters like well-known glutamate important contribution of activated astroglial cells
transporter 1 (GLT-1) and dynamic diffusion play a in epileptogenesis in the acquired epilepsy, although
physiological modulating role in shaping synaptic epilepsy has long been considered as a disease caused
transmission between neurons. Glutamate action time byabnormal increasing bursts of excitatory neurons,
exclusively. [6,7] In addition, the reactive astrocytes are
Corresponding Author: Dr. Liang-Wei Chen, Institute
of Neurosciences, Department of Neurobiology and characterized with high level of G protein-coupled
Collaborative Innovation Center for Brain Science, The Fourth receptors such as adenosine receptor, which were
Military Medical University, Xi’an 710032, Shaanxi, China.
Email: lwchen@fmmu.edu.cn This is an open access article distributed under the terms of the Creative
Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows
others to remix, tweak, and build upon the work non-commercially, as long as the
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How to cite this article: Chen LW. Astrocyte, reactive astrocytes and
self-regulative apoptosis in the neuroinflammation. Neuroimmunol
Neuroinflammation 2016;3:167-9.
DOI: 10.20517/2347-8659.2016.31
Received: 17-06-2016; Accepted: 22-06-2016
© 2016 Neuroimmunology and Neuroinflammation | Published by OAE Publishing Inc. 167