Spinal microglial β‐endorphin signaling mediates IL‐10 and exenatide‐induced inhibition of synaptic plasticity in neuropathic pain

Ma, Le; Peng, Shi-Yu; Wei, Jinbao; Zhao, Min; Ahmad, Khalil; Chen, Jinghong; Wang, Yongxiang

doi:10.1111/cns.13694

Cited by 22 publications

(15 citation statements)

References 105 publications

(231 reference statements)

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“…It is known that proinflammatory cytokines such as TNF‐α, IL‐1β, and IL‐6 are released in the spinal dorsal horn in response to a variety of pain stimuli. 3 , 39 , 40 , 41 , 42 This was demonstrated in the present study in PSNL mice, which showed increases in all three cytokines. Interestingly, PSNL‐induced increases in the cytokines, in particular TNF‐α and IL‐1β, were reversed by inhibition of PDE4 with either rolipram or roflumilast.…”

Section: Discussionsupporting

confidence: 81%

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Inhibition of phosphodiesterase‐4 in the spinal dorsal horn ameliorates neuropathic pain via cAMP‐cytokine‐Cx43 signaling in mice

et al. 2022

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Section: Discussionsupporting

confidence: 81%

“…It is known that proinflammatory cytokines such as TNF‐α, IL‐1β, and IL‐6 are released in the spinal dorsal horn in response to a variety of pain stimuli 3,39–42 …”

Section: Discussionmentioning

confidence: 99%

Inhibition of phosphodiesterase‐4 in the spinal dorsal horn ameliorates neuropathic pain via cAMP‐cytokine‐Cx43 signaling in mice

et al. 2022

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“…In addition, microglia can modify synaptic activity by releasing molecules such as IL-33 [ 173 ] and IL-1 β [ 55 ]. Alternatively, microglial release of BDNF [ 169 ] or IL-10 [ 178 – 180 ] can also modulate spine formation. Moreover, microglia can modulate spine density by releasing TNF- α [ 181 , 182 ] or IL-10 [ 178 ].…”

Section: Microglial Regulation Of Synapsis Structure and Functionmentioning

confidence: 99%

Fractalkine/CX3CR1-Dependent Modulation of Synaptic and Network Plasticity in Health and Disease

Camacho-Hernández

Peña‐Ortega

2023

Neural Plasticity

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CX3CR1 is a G protein-coupled receptor that is expressed exclusively by microglia within the brain parenchyma. The only known physiological CX3CR1 ligand is the chemokine fractalkine (FKN), which is constitutively expressed in neuronal cell membranes and tonically released by them. Through its key role in microglia-neuron communication, the FKN/CX3CR1 axis regulates microglial state, neuronal survival, synaptic plasticity, and a variety of synaptic functions, as well as neuronal excitability via cytokine release modulation, chemotaxis, and phagocytosis. Thus, the absence of CX3CR1 or any failure in the FKN/CX3CR1 axis has been linked to alterations in different brain functions, including changes in synaptic and network plasticity in structures such as the hippocampus, cortex, brainstem, and spinal cord. Since synaptic plasticity is a basic phenomenon in neural circuit integration and adjustment, here, we will review its modulation by the FKN/CX3CR1 axis in diverse brain circuits and its impact on brain function and adaptation in health and disease.

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“…Recent studies showed that the activation of the GLP1/GLP1R axis improved recognition memory impairment, neuroinflammation, and neurological pain via regulating the AMP-activated protein kinase/nuclear factor kappa B (AMPK/NF-κB) pathway [ 102 , 103 ]. Further, the GLP1R agonist decreases pain hypersensitivity through decreasing pro-inflammatory factors and increasing microglia anti-inflammatory factors, such as interleukin 10 (IL-10), cluster of differentiation 206 (CD206), interleukin 4 (IL-4), and arginase 1 (Arg1) [ 102 , 104 , 105 , 106 , 107 , 108 ]. New research claimed that the gene regulation in response to GLP1R activation is an effective strategy in new treatments for neuropathic pain, by confirming that the GLP1R pathway is involved in pain hypersensitivity mediated by microglia activation [ 109 ].…”

Section: Enteroendocrine Cells In Visceral Pain and Neuropathic Painmentioning

confidence: 99%

Involvement of Intestinal Enteroendocrine Cells in Neurological and Psychiatric Disorders

2022

Biomedicines

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Neurological and psychiatric patients have increased dramatically in number in the past few decades. However, effective treatments for these diseases and disorders are limited due to heterogeneous and unclear pathogenic mechanisms. Therefore, further exploration of the biological aspects of the disease, and the identification of novel targets to develop alternative treatment strategies, is urgently required. Systems-level investigations have indicated the potential involvement of the brain–gut axis and intestinal microbiota in the pathogenesis and regulation of neurological and psychiatric disorders. While intestinal microbiota is crucial for maintaining host physiology, some important sensory and regulatory cells in the host should not be overlooked. Intestinal epithelial enteroendocrine cells (EECs) residing in the epithelium throughout intestine are the key regulators orchestrating the communication along the brain-gut-microbiota axis. On one hand, EECs sense changes in luminal microorganisms via microbial metabolites; on the other hand, they communicate with host body systems via neuroendocrine molecules. Therefore, EECs are believed to play important roles in neurological and psychiatric disorders. This review highlights the involvement of EECs and subtype cells, via secretion of endocrine molecules, in the development and regulation of neurological and psychiatric disorders, including Parkinson’s disease (PD), schizophrenia, visceral pain, neuropathic pain, and depression. Moreover, the current paper summarizes the potential mechanism of EECs in contributing to disease pathogenesis. Examination of these mechanisms may inspire and lead to the development of new aspects of treatment strategies for neurological and psychiatric disorders in the future.

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Spinal microglial β‐endorphin signaling mediates IL‐10 and exenatide‐induced inhibition of synaptic plasticity in neuropathic pain

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 22 publications

References 105 publications

Inhibition of phosphodiesterase‐4 in the spinal dorsal horn ameliorates neuropathic pain via cAMP‐cytokine‐Cx43 signaling in mice

Inhibition of phosphodiesterase‐4 in the spinal dorsal horn ameliorates neuropathic pain via cAMP‐cytokine‐Cx43 signaling in mice

Fractalkine/CX3CR1-Dependent Modulation of Synaptic and Network Plasticity in Health and Disease

Involvement of Intestinal Enteroendocrine Cells in Neurological and Psychiatric Disorders

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