Cited by 67Neuroinflammation and Neurodegeneration MechanismsNeuroscience and Neuropharmacology ResearchPain Mechanisms and Treatments

Glutamate Receptors in Microglia

Murugan, Madhuvika, Ling, Eng-Ang, Kaur, Charanjit·2013·CNS & Neurological Disorders - Drug Targets

Abstract

Expression of functional glutamate receptors (GluR) on glial cells in the developing and mature brain has been recently established. Over the last decade there has been physiological, molecular and biochemical evidence suggesting the presence of GluR on microglia. However, the significance of GluR activation in microglia remains largely unknown. In this review, we discuss the expression of GluR on microglia and the effect of GluR activation on microglial function. Microglia are the resident immune cells of the central nervous system, and activation of GluR in them has been shown to regulate their immunological response which may be either neuroprotective or neurotoxic. Microglial activation is known to initiate a myriad of molecular events such as nitric oxide production, free radicals generation, disruption of calcium regulation and release of proinflammatory cytokines, proteases, neurotransmitters, and excitatory amino acids, primarily glutamate. Since microglial activation has been implicated in several neuropathologies, an understanding of the pathway coupled to the various microglial GluR will help to develop therapeutic interventions for ameliorating microglia-mediated damage.

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Crossref · 10.2174/18715273113126660174

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  • Together with microglia, astrocytes constitute the principal defensive system of the CNS and respond to damage-related stimuli including Aβ and glutamate overload in a process known as astrocyte reactivity.

    “Together with microglia, astrocytes constitute the principal defensive system of the CNS [37], responding to numerous damage‐related stimuli [6, 7, 8, 9] including amyloid β peptides (Aβ) and glutamate overload, in a process known as astrocyte reactivity [15, 37, 38, 39, 40].”
  • Hyperactivated astrocytes and microglia support excitotoxicity through the exacerbated release of glutamate in response to Aβ, and GABA‐producing astrocytes are commonly found in AD.

    “hyperactivated astrocytes and microglia, support excitotoxicity through the exacerbated release of glutamate in response to Aβ [37, 38, 40, 43, 50, 51, 117, 118], and even GABA‐producing astrocytes are commonly found in AD [42, 97, 119].”

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Cited by 67

Authors
Murugan, M., Ling, E.-A., & Kaur, C.
Affiliations
National University of Singapore (SG)
Venue
CNS & Neurological Disorders - Drug Targets
Published
2013-08-31
Volume
12
Issue
6
Pages
773-784
ISSN
  • 1568-007X (ISSN-L)
  • 1871-5273
OpenAlex
W2138084026
Cited by
67
References
0
Citations by year
2026: 2 · 2025: 6 · 2024: 7 · 2023: 6 · 2022: 6 · 2021: 7 · 2020: 5 · 2019: 8 · 2018: 6 · 2017: 4 · 2016: 3 · 2015: 5 · 2014: 1 · 2013: 1
FWCI
1.86
Type
journal article
Language
en
Open access
closed
Locations
  • CNS & Neurological Disorders - Drug Targets (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
Keywords
glutamate receptors, microglia, microglial activation, neuroinflammation, neuroprotection, neurotoxicity, nitric oxide, inflammatory cytokines, excitatory amino acids, glutamate, neuropathology, calcium regulation, free radicals
MeSH terms
Animals, Free Radicals, Humans, Cytokines, Receptors, Glutamate, Microglia, Glutamic Acid

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