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Astrocyte, reactive astrocytes and self-regulative apoptosis in the neuroinflammation
Author(s) -
Liang-Wei Chen
Publication year - 2016
Publication title -
neuroimmunology and neuroinflammation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.125
H-Index - 4
eISSN - 2349-6142
pISSN - 2347-8659
DOI - 10.20517/2347-8659.2016.31
Subject(s) - medicine , neuroinflammation , astrocyte , publishing , neuroscience , immunology , central nervous system , biology , inflammation , political science , law
Received: 17-06-2016; Accepted: 22-06-2016 Astrocyte, one of the most abundant glial cell types, actively functions in stabilizing neural circuits and synaptic transmission in the central nervous system (CNS). Astrocytes not only provide metabolic and trophic supports to various CNS neurons and but also actively work in assisting synaptic transmission and plasticity. A line of growing evidences have documented that astrocytes present as an essential coordinatorin neural circuit function.[1] Firstly, calcium signaling or calcium wave calcium (Ca2+) between neighboring astrocytes contribute to establishment of a huge astrocytic glial network by gap-junctions, which has updated the understanding of astrocyte function in CNS, and led to an idea that astrocytes are powerful regulators of neuronal spiking, synaptic plasticity and brain blood flow as well.[2] The Ca2+ wave in astrocyte processes may also precede onset of hyperemia and function as regulators of neurovascular coupling.[3] Secondly, astrocytes can also fast respond to sensory stimulation and involve in generation of neuronal rhythmic activity, and blockade with a Ca2+ chelator can sufficiently prevent neurons from a rhythmic bursting, indicating that astrocytes partially and critically contribute a fundamental neuronal firingpattern or generation of rhythmic activity.[4] Thirdly, distinct astrocytic transporters like well-known glutamate transporter 1 (GLT-1) and dynamic diffusion play a physiological modulating role in shaping synaptic transmission between neurons. Glutamate action time in synaptic transmission is controlled by the astrocytic GLT-1, i.e. while impairing GLT-1 diffusion could slow kinetics of excitatory currents or prolonged time course of synaptic glutamate transmission.[5]

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