Glutamate Receptors in Microglia
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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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].”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp><i>APOE3</i></scp> Christchurch homozygote glioprotection (2023) · cites this paper as [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].”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp><i>APOE3</i></scp> Christchurch homozygote glioprotection (2023) · cites this paper as [40]
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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
- Publisher
- Bentham Science Publishers Ltd.
- 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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