Journal
MOLECULAR NEUROBIOLOGY
Volume 56, Issue 7, Pages 5202-5228Publisher
SPRINGER
DOI: 10.1007/s12035-018-1428-7
Keywords
Microglia; Brain injury; Receptors
Categories
Funding
- US Army Medical Research and Material Command [W81XWH-15-1-0303]
- New Jersey Commission for Brain Injury Research [CBIR17PIL020]
- Rutgers Brain Health Institute [BHI-RUN-NJIT-2016]
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Microglia have been implicated as a key mediator of chronic inflammation following traumatic brain injury (TBI). The animal models of TBI vary significantly based on the type of brain injury (focal versus diffuse). This has made it extremely difficult to assess the role of microglia and the window of microglia activation. Hence, the focus of this review is to summarize the time course ofmicroglia activation in various animal models of TBI. The review explores the repertoire of secondary injurymechanisms such as aberrant neurotransmitter release, oxidative stress, blood-brain barrier disruption, and production of pro-inflammatory cytokines that follow microglia activation. Since receptors act as sensors for activation, we highlight certain microglia receptors that have been implicated in TBI pathology, including fractalkine receptor (CX3CR1), purinergic receptor (P2Y12R), Toll-like receptor (TLR4), scavenger receptors, tumor necrosis factor receptor (TNF-1R), interleukin receptor (IL-1R), complement receptors, and peroxisome proliferator-activated receptor (PPAR). In addition to describing their downstream signaling pathways in TBI, we describe the functional consequences of their activation and the implication in behavioral outcomes. Taken together, this review will provide a holistic view of the role of microglia and its receptors in TBI based on animal studies.
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