Intravenous lidocaine alleviates postherpetic neuralgia in rats via regulation of neuroinflammation of microglia and astrocytes

Ma, Lulin; Li, Juan; Zhou, Junli; Zhang, Dexin; Xiao, Zhi; Yu, Tian; Liu, Ying; Cao, Song

doi:10.1016/j.isci.2021.102108

Cited by 24 publications

(26 citation statements)

References 58 publications

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“…It is suggested that LC:SC activation reduces the production of pro-inflammatory cytokines by inhibiting glial cell activation. It is widely reported that occurrence of NP is often accompanied by the activation of glial cells, and the activated glial cells can release various pro-inflammatory cytokines (such as TNF-α, IL-1β, and IL-6), anti-inflammatory cytokines (such as IL-4, Arg1, and IL-10), and various analgesic and pain-causing substances [ 54 , 55 ]. The pro-inflammatory glial mediators regulate excitatory and inhibitory synaptic transmission in the spinal cord by enhancing nociceptive neurotransmission, which ultimately leads to central sensitization [ 56 , 57 ].…”

Section: Discussionmentioning

confidence: 99%

Activation of locus coeruleus-spinal cord noradrenergic neurons alleviates neuropathic pain in mice via reducing neuroinflammation from astrocytes and microglia in spinal dorsal horn

Wei

Zhou

et al. 2022

J Neuroinflammation

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Background The noradrenergic neurons of locus coeruleus (LC) project to the spinal dorsal horn (SDH), and release norepinephrine (NE) to inhibit pain transmission. However, its effect on pathological pain and the cellular mechanism in the SDH remains unclear. This study aimed to explore the analgesic effects and the anti-neuroinflammation mechanism of LC-spinal cord noradrenergic pathway (LC:SC) in neuropathic pain (NP) mice with sciatic chronic constriction injury. Methods The Designer Receptors Exclusively Activated by Designer Drugs (DREADD) was used to selectively activate LC:SC. Noradrenergic neuron-specific retro–adeno-associated virus was injected to the spinal cord. Pain threshold, LC and wide dynamic range (WDR) neuron firing, neuroinflammation (microglia and astrocyte activation, cytokine expression), and α2AR expression in SDH were evaluated. Results Activation of LC:SC with DREADD increased the mechanical and thermal nociceptive thresholds and reduced the WDR neuron firing. LC:SC activation (daily, 7 days) downregulated TNF-α and IL-1β expression, upregulated IL-4 and IL-10 expression in SDH, and inhibited microglia and astrocytes activation in NP mice. Immunofluorescence double staining confirmed that LC:SC activation decreased the expression of cytokines in microglia of the SDH. In addition, the effects of LC:SC activation could be reversed by intrathecal injection of yohimbine. Immunofluorescence of SDH showed that NE receptor α2B-AR was highly expressed in microglia in CCI mice. Conclusion These findings indicate that selective activation of LC:SC alleviates NP in mice by increasing the release of NE and reducing neuroinflammation of astrocytes and microglia in SDH.

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Section: Discussionmentioning

confidence: 99%

Activation of locus coeruleus-spinal cord noradrenergic neurons alleviates neuropathic pain in mice via reducing neuroinflammation from astrocytes and microglia in spinal dorsal horn

Wei

Zhou

et al. 2022

J Neuroinflammation

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“…In the process of pain recognition, multiple brain regions were activated at the same time, while the activation of microglia in the prefrontal cortex (PFC), the anterior cingulate cortex (ACC), 22 and the hippocampus 21,23 may be responsible for persistent neuropathic pain. The activated microglia promote the release of proinflammatory cytokines, induce neuroinflammation, and enhance long‐term noxious nerve signal transmission, leading to central pain sensitization, causing and aggravating neuropathic pain 20 . After peripheral nerve injury (PNI), TNF‐α can differentially regulate hippocampus and spinal cord synaptic plasticity through a microglia‐dependent mechanism 23 .…”

Section: Ne Regulates Inflammatory Activation Of Microgliamentioning

confidence: 99%

“…More evidence of functional magnetic resonance imaging studies in patients with postherpetic neuralgia (PHN) suggests that there are abnormal functional activities in the regions of the brain linked to anxiety and depression 41 . Most PHN patients also have anxiety and depression that may be related to the activation of microglia at the PFC, ACC, and hippocampus 20 . Negrete et al injected intra‐articular sodium iodoacetate in kappa opioid receptor knockout mice, predynorphin knockout mice, and wild‐type mice to induce osteoarthritis; the results showed that all mice had abnormal pain, and the activation of microglia in the spinal cord and lumbar showed a similar increase.…”

Section: Microglia Lc–noradrenergic System and Anxiety/depressionmentioning

confidence: 99%

Effects of norepinephrine on microglial neuroinflammation and neuropathic pain

Zou

Zhou

et al. 2021

Ibrain

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Norepinephrine (NE) is an important neurotransmitter in the central nervous system. NE is released from locus coeruleus neurons and is involved in a variety of physiological and pathological processes. Neuroinflammation is a common manifestation of many kinds of neurological diseases. The activation of microglia directly affects the status of neuroinflammation. Several kinds of adrenergic receptors, which anchor on microglia and can be regulated by NE, affect the activation of microglia and neuroinflammation. NE influences chronic pain, anxiety, and depression by regulating the activation of microglia.

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“…Nevertheless, previous studies showed multivariate results of the cortex in PTSD models. In an early-life stress and herpes zoster pain model, microglia in the PFC is markedly activated ( Ma et al, 2021 ; Usui et al, 2021 ). Neuroinflammation originating from microglia in the medial PFC induced by chronic stress, leading to depressive-like behavior ( Kitaoka, 2022 ).…”

Section: Discussionmentioning

confidence: 99%

S-Ketamine Pretreatment Alleviates Anxiety-Like Behaviors and Mechanical Allodynia and Blocks the Pro-inflammatory Response in Striatum and Periaqueductal Gray From a Post-traumatic Stress Disorder Model

Yang

et al. 2022

Front. Behav. Neurosci.

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This study aims to explore the regulatory effect of S-ketamine on the mechanical allodynia, anxiety-like behaviors and microglia activation in adult male rats exposed to an animal model of post-traumatic stress disorder (PTSD). The rat PTSD model was established by the exposure to single-prolonged stress (SPS), and 1 day later, rats were intraperitoneally injected with 5 mg/kg S-ketamine or normal saline, respectively. Paw withdrawal mechanical threshold was measured 2 days before, and 1, 3, 5, 7, 10, 14, 21 and 28 days after injection to assess mechanical allodynia in the SPS-exposed rats. For anxiety-like behaviors, the open field test and elevated plus maze test were performed at 7 and 14 days after S-ketamine treatment in the SPS-exposed rats, respectively. SPS-induced rats presented pronounced mechanical allodynia and anxiety-like behaviors, which were alleviated by S-ketamine treatment. After behavioral tests, rats were sacrificed for collecting the anterior cingulate cortex (ACC), prefrontal cortex (PFC), dorsal striatum, and periaqueductal gray (PAG). Protein levels of TNF-α, IL-1β, p-NF-κB, and NF-κB in brain regions were examined by Western blot. In addition, microglia activation in each brain region was determined by immunofluorescence staining of the microglia-specific biomarker Iba-1. Interestingly, pro-inflammatory cytokines were significantly upregulated in the dorsal striatum and PAG, rather than ACC and PFC. Activated microglia was observed in the dorsal striatum and PAG as well, and upregulated p-NF-κB was detected in the dorsal striatum. Inflammatory response, phosphorylation of NF-κB and microglia activation in certain brain regions were significantly alleviated by S-ketamine treatment. Collectively, S-ketamine is a promising drug in alleviating mechanical allodynia, anxiety-like behaviors, and pro-inflammatory responses in discrete brain regions in a model of PTSD.

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Intravenous lidocaine alleviates postherpetic neuralgia in rats via regulation of neuroinflammation of microglia and astrocytes

Cited by 24 publications

References 58 publications

Activation of locus coeruleus-spinal cord noradrenergic neurons alleviates neuropathic pain in mice via reducing neuroinflammation from astrocytes and microglia in spinal dorsal horn

Activation of locus coeruleus-spinal cord noradrenergic neurons alleviates neuropathic pain in mice via reducing neuroinflammation from astrocytes and microglia in spinal dorsal horn

Effects of norepinephrine on microglial neuroinflammation and neuropathic pain

S-Ketamine Pretreatment Alleviates Anxiety-Like Behaviors and Mechanical Allodynia and Blocks the Pro-inflammatory Response in Striatum and Periaqueductal Gray From a Post-traumatic Stress Disorder Model

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