Citation

Younger D, Murugan M, Rama Rao KV, Wu LJ, Chandra N. Mol. Neurobiol. 2019; 56(7): 5202-5228.

Affiliation

Department of Bioengineering, New Jersey Institute of Technology, 111 Lock Street, Room105 CHEN bldg, Newark, NJ, 07102, USA. namas.chandra@njit.edu.

Copyright

(Copyright © 2019, Springer)

DOI

10.1007/s12035-018-1428-7

PMID

30554385

Abstract

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 of microglia activation in various animal models of TBI. The review explores the repertoire of secondary injury mechanisms 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.

Language: en

Keywords

Brain injury; Microglia; Receptors