Morphine Induces Upregulation of Neuronally Expressed CB2 Receptors in the Spinal Dorsal Horn of Rats

Grenier, Patrick; Sunavsky, Adam; Olmstead, Mary C.

doi:10.1089/can.2020.0004

Cited by 5 publications

(2 citation statements)

References 47 publications

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“…Börner reported that CB2 receptor agonist JWH015 increased the mRNA expression of MOR dependent on the CB2 receptor ( Börner et al, 2006 ). Morphine also induced upregulation of neuronal expressed CB2 receptor in the spinal cord ( Grenier et al, 2021 ). CB2 receptor and MOR might coexpression in the nervous system through previous studies.…”

Section: Discussionmentioning

confidence: 99%

The effect of cannabinoid type 2 receptor agonist on morphine tolerance

Cui,

Zhang,

Zhang

2024

IBRO Neuroscience Reports

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Section: Discussionmentioning

confidence: 99%

The effect of cannabinoid type 2 receptor agonist on morphine tolerance

Cui,

Zhang,

Zhang

2024

IBRO Neuroscience Reports

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“…Converging evidence indicates that CB2Rs play an important role in regulating chronic pain states, although their exact expression pattern has been a topic of intense debate (Rogers, 2015). Resting microglia typically express low levels of CB2R (Duffy et al, 2021), but this expression is markedly increased in inflammatory and neuropathic pain states (Zhang et al, 2003;Walczak et al, 2006;Romero-Sandoval and Eisenach, 2007;Racz et al, 2008b;Brownjohn and Ashton, 2012;Naguib et al, 2012;Shiue et al, 2017;Grenier et al, 2021). The extent of this CB2R increase appears to be dependent on the pain model used (Zhang et al, 2003) and may promote microglia to switch toward a more anti-inflammatory phenotype (Bie et al, 2018;Komorowska-Muller and Schmole, 2020).…”

Section: Microglial Cb2r In Nociceptive Signalingmentioning

confidence: 99%

Cannabinoids in Chronic Pain: Therapeutic Potential Through Microglia Modulation

Hoogen

Harding

Davidson

et al. 2022

Front. Neural Circuits

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Chronic pain is a complex sensory, cognitive, and emotional experience that imposes a great personal, psychological, and socioeconomic burden on patients. An estimated 1.5 billion people worldwide are afflicted with chronic pain, which is often difficult to treat and may be resistant to the potent pain-relieving effects of opioid analgesics. Attention has therefore focused on advancing new pain therapies directed at the cannabinoid system because of its key role in pain modulation. Endocannabinoids and exogenous cannabinoids exert their actions primarily through Gi/o-protein coupled cannabinoid CB1 and CB2 receptors expressed throughout the nervous system. CB1 receptors are found at key nodes along the pain pathway and their activity gates both the sensory and affective components of pain. CB2 receptors are typically expressed at low levels on microglia, astrocytes, and peripheral immune cells. In chronic pain states, there is a marked increase in CB2 expression which modulates the activity of these central and peripheral immune cells with important consequences for the surrounding pain circuitry. Growing evidence indicate that interventions targeting CB1 or CB2 receptors improve pain outcomes in a variety of preclinical pain models. In this mini-review, we will highlight recent advances in understanding how cannabinoids modulate microglia function and its implications for cannabinoid-mediated analgesia, focusing on microglia-neuron interactions within the spinal nociceptive circuitry.

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Synthetic cannabinoids reduce the inflammatory activity of microglia and subsequently improve neuronal survival in vitro

Young

Denovan‐Wright

2022

Brain, Behavior, and Immunity

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Morphine Induces Upregulation of Neuronally Expressed CB2 Receptors in the Spinal Dorsal Horn of Rats

Cited by 5 publications

References 47 publications

The effect of cannabinoid type 2 receptor agonist on morphine tolerance

The effect of cannabinoid type 2 receptor agonist on morphine tolerance

Cannabinoids in Chronic Pain: Therapeutic Potential Through Microglia Modulation

Synthetic cannabinoids reduce the inflammatory activity of microglia and subsequently improve neuronal survival in vitro

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