Microglia: Activation and Their Significance in the Central Nervous System

Abstract

Microglia are resident monocyte-lineaged cells in the brain. Their characteristic feature is that they react to injury and diseases of the brain and become morphologically and functionally activated. Although some trigger molecules which activate microglia are predicted to be released from injured or affected cells, such molecules have not yet been identified. The main role of activated microglia is believed to be in brain defense, as scavengers of dead cells, and as immune or immunoeffector cells. Recent biochemical and neurobiological studies have further indicated that they significantly affect the pathological state and/or regulate the regenerative state and remodeling of the brain by producing a variety of biologically active molecules including cytotoxic and neurotrophic molecules.

MMHD [(S,E)-2-Methyl-1-(2-methylthiazol-4-yl) hexa-1,5-dien-ol], a Novel Synthetic Compound Derived From Epothilone, Suppresses Nuclear Factor-κB–Mediated Cytokine Expression in Lipopolysaccharide-Stimulated BV-2 Microglia

“…Microglia activation has both beneficial and harmful effects on neuronal cell survival (32). However, accumulated experimental results indicate that microglial activation is more associated with neurodegenerative diseases (33).…”

Do glial cells control pain?

“…They originate from bone marrow-derived monocytes migrating during perinatal time (Nakajima & Kohsaka, 2001). Quiescent microglia are not passive cells but rather actively sense their environment with their ramified processes (Nimmerjahn et al, 2005;Raivich, 2005;Hanisch and Kettenmann, 2007).…”

Stereological and somatotopic analysis of the spinal microglial response to peripheral nerve injury

“…PNI induces a marked microglial reaction in the dorsal horn of the spinal cord. Microglia respond with a stereotypical 'activation'-their numbers swell through proliferation and infiltration and they change their morphology from the characteristic ramified 'resting' state to the more amoeboid 'activated' state, a process also associated with considerable change in gene expression (Perry, 1994;Kreutzberg, 1996;Stoll and Jander, 1999;Nakajima and Kohsaka, 2001). This 'activation' response has been reported in all experimental models of neuropathic pain involving peripheral nerve injury (Liu et al, 1995;Coyle, 1998;Colburn et al, 1999;Herzberg and Sagen, 2001;Tsuda et al, 2003;Zhang and De Koninck, 2006).…”