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http://nro.sagepub.com/content/20/2/160?etoc
- 1Department of Neurobiology and Brain Research Institute, University of California, Los Angeles, CA, USA
- Michael V. Sofroniew, Department of Neurobiology, David Geffen School of Medicine, University of California, Los Angeles, 10833 Le Conte Avenue, Los Angeles, CA 90095-1763, USA. Email: sofroniew@mednet.ucla.edu
Abstract
Astrocytes are increasingly recognized as
exerting complex functions essential for normal neural activity in the
healthy central
nervous system (CNS). Because astrocytes also
respond to all forms of CNS injury or disease, there is growing interest
in
how reactive astrogliosis might alter astrocyte
functions and thereby affect neural functions. Reactive astrogliosis is
heterogeneous
and regulated in a context specific manner by
different molecular signals. Prominent among astrocyte signaling
mechanisms
is the ability to respond to, as well as to
produce, many different cytokines and inflammatory mediators. These
signaling
mechanisms enable astrocytes to interact with
diverse cell types in ways that may contribute to crosstalk between
immune/inflammatory
and neural systems. Consistent with this notion is
the increasing evidence that cytokines and inflammatory mediators
modulate
astrocyte signaling not only to influence immune
and inflammatory activities in the CNS, but also to influence synaptic
and
neural functions in ways that may affect complex
behaviors such as sickness behavior, pain, appetite, sleep, and mood.
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