http://www.sciencedirect.com/science/article/pii/S0014488615000898
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- Astrocytes respond to diverse forms of brain injury with heterogeneous and progressive changes of gene expression, morphology, proliferative capacity and function that are collectively referred to as reactive astrogliosis.
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- In response to TBI, astrocytes in different cellular microenvironments tune their reactivity to varying degrees of axonal injury, vascular disruption, ischemia and inflammation.
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- TBI-reactive astrocytes significantly contribute to post-traumatic tissue repair and synaptic remodeling following brain trauma.
Abstract
Astrocytes
sense changes in neural activity and extracellular space composition.
In response, they exert homeostatic mechanisms critical for maintaining
neural circuit function, such as buffering neurotransmitters, modulating
extracellular osmolarity and calibrating neurovascular coupling. In
addition to upholding normal brain activities, astrocytes respond to
diverse forms of brain injury with heterogeneous and progressive changes
of gene expression, morphology, proliferative capacity and function
that are collectively referred to as reactive astrogliosis. Traumatic
brain injury (TBI) sets in motion complex events in which noxious
mechanical forces cause tissue damage and disrupt central nervous system
(CNS) homeostasis, which in turn trigger diverse multi-cellular
responses that evolve over time and can lead either to neural repair or
secondary cellular injury. In response to TBI, astrocytes in different
cellular microenvironments tune their reactivity to varying degrees of
axonal injury, vascular disruption, ischemia and inflammation. Here we
review different forms of TBI-induced astrocyte reactivity and the
functional consequences of these responses for TBI pathobiology.
Evidence regarding astrocyte contribution to post-traumatic tissue
repair and synaptic remodeling is examined, and the potential for
targeting specific aspects of astrogliosis to ameliorate TBI sequelae is
considered.
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