Research Topic

Microglia: Mediators of Immune, Aminergic, Growth Factors and HPA Axis Pathways in the Brain

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Microglia are small glial cells in the brain and spinal cord that remain in the quiescent state under basal condition maintaining homeostasis but becomes elongated with oblong nuclei (activated state) during brain pathologies and neurodegenerative diseases. They are the most mobile of all glial cells, ...

Microglia are small glial cells in the brain and spinal cord that remain in the quiescent state under basal condition maintaining homeostasis but becomes elongated with oblong nuclei (activated state) during brain pathologies and neurodegenerative diseases. They are the most mobile of all glial cells, proliferate extensively, migrate fast and phagocytoses the pathogens and stress associated proteins to clear the infected tissues. Microglia regulate the extensive bi-directional communication between the nervous and the immune systems in response to different immunological, physiological and psychological stressors. The immune effector activity of microglia in the CNS during pathological conditions, such as psychological stress, pathological ageing, chronic infections, immune reaction such as in Multiple Sclerosis has attracted attention from researchers. While the microglial response to injury and pathogens are extensively studied, their role in neurodegenerative processes and various psychiatric conditions remain unclear. Interestingly, there are evidence suggesting that microglia also mediate non-immune related mechanisms, such as aminergic, growth factors and HPA axis pathways.

Microglia express receptors for serotonin, for example, 5-HT2A, 5-HT2B and 5-HT4. Serotonin interacts with microglial cells and participates in the microglial immune functions, for example, serotonin has been shown to suppress IFN-γ-induced phagocytosis, MHC class II expression and interaction between monocytes and NK cells. Microglia also expresses receptors for GABA which when stimulated attenuate the proinflammatory functions of microglia. Similarly, histamine deficiency reduces ramifications of microglia in the striatum and the hypothalamus, however, the exact mechanism through which histamine interacts with microglia remains unclear. Microglia are also responsible for the selective depletion of nigral dopamine during Parkinson’s disease. All above evidence point at the neurotransmitter-dependent signalling pathways in microglial cells under inflammatory conditions.

Until recently, microglial cells were ignored to be a part of the neurogenic niche. However, microglia secrete growth factors such as NGF and insulin-like growth factor thus participating in neuronal survival and neuronal repair processes. On the contrary, fibroblast growth factor induces microglial proliferation and morphological changes, which is similar to the response of microglia to injuries and infections. NGF, NT-3 and BDNF may also regulate microglial dynamics as they all have been shown to promote proliferation of microglia and regulate microglial MHC class II expression, thereby influencing the surrounding milieu during neuronal regeneration.

Microglial cells predominantly express glucocorticoid receptors (GR) in the CNS. Through these key innate immune cells, glucocorticoids perform major regulatory functions on the innate immune system of the CNS in health and disease. Microglia GR signalling was recently found to suppress the priming effects of chronic stress on microglia reactivity. In contrast, the cytokines secreted by microglia, for example, TNF-α and IL-1β, have been shown to hamper the activation of the HPA axis and the subsequent release of glucocorticoids.

The multidimensional roles of microglia in the brain therefore makes them the cells of interest for future research on CNS disorders. Here, we invite manuscripts discussing and reporting the roles of microglia at the centre of immune and non-immune processes in the brain with the aim of broadening research knowledge base.


Keywords: microglia, neuroimmunology, neurobiology, mental illness, stress response


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15 December 2018 Manuscript
30 April 2019 Manuscript Extension

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Topic Editors

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Submission Deadlines

15 December 2018 Manuscript
30 April 2019 Manuscript Extension

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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