Activation of murine microglial N9 cells is attenuated through cannabinoid receptor CB2 signaling

Ma, Lei; Jia, Ji-dong; Liu, Xiangyu; Bai, Feihu; Wang, Qiang; Xiong, Lize

doi:10.1016/j.bbrc.2015.01.073

Cited by 72 publications

(54 citation statements)

References 34 publications

(36 reference statements)

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“…These effects are reversed by inhibition of CB2R or absent in CB2R knockout mice 34. Pretreatment with AM1241, another CB2 agonist, has also been reported to attenuate LPS plus interferon γ (IFNγ)-induced microglial activation by shifting microglial polarisation from the toxic M1 state to the protective M2 state 35. In models of Alzheimer's disease, the endocannabinoid system may be similarly protective.…”

Section: Cannabinoid Microglial Receptorsmentioning

confidence: 99%

Neurotransmitter receptors on microglia

2016

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As the resident immune cells in the central nervous system, microglia have long been hypothesised to promote neuroinflammation and exacerbate neurotoxicity. However, this traditional view has undergone recent revision as evidence has accumulated that microglia exert beneficial and detrimental effects depending on activation status, polarisation phenotype and cellular context. A variety of neurotransmitter receptors are expressed on microglia and help mediate the bidirectional communication between neurons and microglia. Here we review data supporting the importance of neurotransmitter receptors on microglia, with a special emphasis on glutamate, γ-aminobutyric acid (GABA), norepinephrine, cannabinoid and acetylcholine receptors. We summarise evidence favouring a significant role for neurotransmitter receptors in modulating microglial activation, phagocytic clearance and phenotypic polarisation. Elucidating the effects of neurotransmitter receptors on microglia and dissecting the underlying mechanisms may help accelerate the discovery of novel drugs that tap the therapeutic potential of microglia.

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Section: Cannabinoid Microglial Receptorsmentioning

confidence: 99%

Neurotransmitter receptors on microglia

2016

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“…Lipopolysaccharide induces “sickness behavior” in rodents, a syndrome that shows some similarity with depressive symptoms and depends on prolonged cytokines release and microglial activation ( 123 , 124 ). Accordingly, using LPS as inflammatory stimulus, cannabinoids reduced the number of circulating lymphocyte, corticosterone levels ( 125 ), and the release of IL-1β, TNF-α, and iNOS expression in vitro ( 126 ). Moreover, the long-lasting behavioral deficits induced by LPS are prevented by the administration of THC ( 127 ) or cannabidiol (CBD) ( 108 ).…”

Section: Cannabinoids As Immunomodulators In the Central Nervous Systmentioning

confidence: 99%

Microglial Cells as a Link between Cannabinoids and the Immune Hypothesis of Psychiatric Disorders

et al. 2016

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Psychiatric disorders are one of the leading causes of disability worldwide. Although several therapeutic options are available, the exact mechanisms responsible for the genesis of these disorders remain to be fully elucidated. In the last decade, a body of evidence has supported the involvement of the immune system in the pathophysiology of these conditions. Microglial cells play a significant role in maintaining brain homeostasis and surveillance. Dysregulation of microglial functions has been associated with several psychiatric conditions. Cannabinoids regulate the brain–immune axis and inhibit microglial cell activation. Here, we summarized evidence supporting the hypothesis that microglial cells could be a target for cannabinoid influence on psychiatric disorders, such as anxiety, depression, schizophrenia, and stress-related disorders.

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“…In this study, we used lipopolysaccharide (LPS) plus interferon gamma (IFN γ ), two proinflammatory substances, to activate N9 microglial cells [21], and took resveratrol to decrease the activation of the cells. We hypothesized that resveratrol can decrease the activation of N9 microglial cells exposed to LPS plus IFN γ , and microglial SIRT1-SOCS1 pathway may mediate the anti-inflammatory process of resveratrol.…”

Section: Introductionmentioning

confidence: 99%

Resveratrol Attenuates Microglial Activation via SIRT1‐SOCS1 Pathway

Zhang

Liu

et al. 2017

Evidence-Based Complementary and Alternative Medicine

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Microglial activation is involved in a variety of neurological disorders, and overactivated microglial cells can secrete large amount of proinflammatory factors and induce neuron death. Therefore, reducing microglial activation is believed to be useful in treating the disorders. In this study, we used 10 ng/ml lipopolysaccharide plus 10 U/ml interferon γ (LPS/IFNγ) to induce N9 microglial activation and explored resveratrol- (RSV-) induced effects on microglial activation and the underlying mechanism. We found that LPS/IFNγ exposure for 24 h increased inducible nitric oxide synthase (iNOS) and nuclear factor κB (NF-κB) p65 subunit expressions in the cells and enhanced tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β) releases from the cells. RSV of 25 μM reduced the iNOS and NF-κB p65 subunit expressions and the proinflammatory factors' releases; the knockdown of silent information regulator factor 2-related enzyme 1 (SIRT1) or suppressor of cytokine signaling 1 (SOCS1) by using the small interfering RNA, however, significantly abolished the RSV-induced effects on iNOS and NF-κB p65 subunit expressions and the proinflammatory factors' releases. These findings showed that microglial SIRT1-SOCS1 pathway may mediate the RSV-induced inhibition of microglial activation in the LPS/IFNγ-treated N9 microglia.

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Activation of murine microglial N9 cells is attenuated through cannabinoid receptor CB2 signaling

Cited by 72 publications

References 34 publications

Neurotransmitter receptors on microglia

Neurotransmitter receptors on microglia

Microglial Cells as a Link between Cannabinoids and the Immune Hypothesis of Psychiatric Disorders

Resveratrol Attenuates Microglial Activation via SIRT1‐SOCS1 Pathway

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