Histamine Modulation of Acute Nociception Involves Regulation of Na<sub>v</sub>1.8 in Primary Afferent Neurons in Mice

Yu, Jie; Lou, Guo Dong; Shou, Wen Ting; Jia, Yue; Tang, Ying; Hou, Wanwan; Xu, Tian; Ohtsu, Hiroshi; Zhang, Shi Hong; Chen, Zhong

doi:10.1111/cns.12134

Cited by 8 publications

(6 citation statements)

References 36 publications

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“…Interestingly, this increased expression was inhibited only by H2 receptor blockers (e.g., famotidine) and not by antagonists of H1 or H3 receptors. These findings are consistent with those of Yu et al [122]. …”

Section: How Do Pharmacological Interventions Take Advantage Of Pasupporting

confidence: 94%

Transmission pathways and mediators as the basis for clinical pharmacology of pain

Kirkpatrick

McEntire

Smith

et al. 2016

Expert Review of Clinical Pharmacology

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Introduction Mediators in pain transmission are the targets of a multitude of different analgesic pharmaceuticals. This review explores the most significant mediators of pain transmission as well as the pharmaceuticals that act on them. Areas Covered The review explores many of the key mediators of pain transmission. In doing so, this review uncovers important areas for further research. It also highlights agents with potential for producing novel analgesics, probes important interactions between pain transmission pathways that could contribute to synergistic analgesia, and emphasizes transmission factors that participate in transforming acute injury into chronic pain. Expert Commentary This review examines current pain research, particularly in the context of identifying novel analgesics, highlighting interactions between analgesic transmission pathways, and discussing factors that may contribute to the development of chronic pain after an acute injury.

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Section: How Do Pharmacological Interventions Take Advantage Of Pasupporting

confidence: 94%

Transmission pathways and mediators as the basis for clinical pharmacology of pain

Kirkpatrick

McEntire

Smith

et al. 2016

Expert Review of Clinical Pharmacology

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“…Itch and pain are two distinct somatic sensations, but they also share many similarities [4;18;29;34;36;47;68;69]. Itch evokes scratching response, while pain elicits withdrawal reflex [22].…”

Section: Introductionmentioning

confidence: 99%

Toll-like receptor 4 contributes to chronic itch, alloknesis, and spinal astrocyte activation in male mice

Liu

Han

Chen

et al. 2016

Pain

120

155

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Increasing evidence suggests that Toll-like receptor 4 (TLR4) contributes importantly to spinal cord glial activation and chronic pain sensitization; however, its unique role in acute and chronic itch is unclear. In this study, we investigated the involvement of TLR4 in acute and chronic itch models in male mice using both transgenic and pharmacological approaches. Tlr4−/− mice exhibited normal acute itch induced by compound 48/80 and chloroquine, but these mice showed substantial reductions in scratching in chronic itch models of dry skin, induced by acetone and diethyether followed by water (AEW), contact dermatitis, and allergic contact dermatitis on the neck. Intrathecal (spinal) inhibition of TLR4 with lipopolysaccharide Rhodobacter sphaeroides (LPS-RS) did not affect acute itch but suppressed AEW-induced chronic itch. Compound 48/80 and AEW also produced robust alloknesis, a touch-elicited itch in wild-type mice, which was suppressed by intrathecal LPS-RS and Tlr4−/− deletion. AEW induced persistent upregulation of Tlr4 mRNA and increased TLR4 expression in GFAP-expressing astrocytes in spinal cord dorsal horn. AEW also induced TLR4-dependent astrogliosis (GFAP upregulation) in spinal cord. Intrathecal injection of astroglial inhibitor L-α-aminoadipate reduced AEW-induced chronic itch and alloknesis without affecting acute itch. Spinal TLR4 was also necessary for AEW-induced chronic itch in the cheek model. Interestingly, scratching plays an essential role in spinal astrogliosis, since AEW-induced astrogliosis was abrogated by putting Elizabethan Collars on the neck to prevent scratching the itchy skin. Our findings suggest that spinal TLR4 signaling is important for spinal astrocyte activation and astrogliosis that may underlie alloknesis and chronic itch.

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“…However, the role of histamine in neuropathic pain is not fully understood yet. Previously, we reported that, for the first time, histamine might regulate Nav1.8 expression under physiological condition , whereas whether histamine regulates Nav1.8 expression after nerve injury remains unclear. Therefore, the present study was designed to investigate the effect of histamine on Nav1.8 expression in primary afferent neurons in vitro and in vivo and the type of histamine receptors that mediates this effect.…”

Section: Introductionmentioning

confidence: 96%

Histamine Upregulates Nav1.8 Expression in Primary Afferent Neurons via H₂ Receptors: Involvement in Neuropathic Pain

Yue

Wang

et al. 2014

CNS Neurosci Ther

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Introduction: The upregulation of Nav1.8 in primary afferents plays a critical role in the development and persistence of neuropathic pain. The mechanisms underlying the upregulation are not fully understood. Aims: The present study aims to investigate the regulatory effect of histamine on the expression of Nav1.8 in primary afferent neurons and its involvement in neuropathic pain. Results: Histamine at 10 À8 M increased the expression of Nav1.8 in cultured DRG neurons. This effect could be blocked by H 2 receptor antagonist cimetidine or famotidine, but not by H 1 receptor antagonist pyrilamine or dual H 3 /H 4 antagonist thioperamide. Peri-sciatic administration of histamine increased Nav1.8 expression in the sciatic nerve and L4/L5 DRG neurons in a dose-dependent manner, accompanied with remarkable mechanical allodynia and heat hyperalgesia in the ipsilateral hindpaw. Famotidine but not pyrilamine or thioperamide inhibited Nav1.8 upregulation and pain hypersensitivity. In addition, famotidine (40 mg/kg, i.p.) not only suppressed autotomy behavior in the rat neuroma model of neuropathic pain but also attenuated mechanical allodynia and thermal hyperalgesia following partial sciatic nerve ligation. Moreover, famotidine inhibited Nav1.8 upregulation in the neuroma and ligated sciatic nerve. Conclusions: Our findings indicate that histamine increases Nav1.8 expression in primary afferent neurons via H 2 receptor-mediated pathway and thereby contributes to neuropathic pain. H 2 receptor antagonists may potentially be used as analgesics for patients with neuropathic pain.

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Histamine Modulation of Acute Nociception Involves Regulation of Na_v1.8 in Primary Afferent Neurons in Mice

Abstract: Our results indicate that histamine participates in acute pain modulation in a dose-related manner. The regulation of Nav 1.8 expression and the excitability of nociceptive primary afferent neurons may be involved in the underlying mechanisms.

Cited by 8 publications

References 36 publications

Transmission pathways and mediators as the basis for clinical pharmacology of pain

Transmission pathways and mediators as the basis for clinical pharmacology of pain

Toll-like receptor 4 contributes to chronic itch, alloknesis, and spinal astrocyte activation in male mice

Histamine Upregulates Nav1.8 Expression in Primary Afferent Neurons via H₂ Receptors: Involvement in Neuropathic Pain

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Histamine Modulation of Acute Nociception Involves Regulation of Nav1.8 in Primary Afferent Neurons in Mice

Abstract: Our results indicate that histamine participates in acute pain modulation in a dose-related manner. The regulation of Nav 1.8 expression and the excitability of nociceptive primary afferent neurons may be involved in the underlying mechanisms.

Cited by 8 publications

References 36 publications

Transmission pathways and mediators as the basis for clinical pharmacology of pain

Transmission pathways and mediators as the basis for clinical pharmacology of pain

Toll-like receptor 4 contributes to chronic itch, alloknesis, and spinal astrocyte activation in male mice

Histamine Upregulates Nav1.8 Expression in Primary Afferent Neurons via H2 Receptors: Involvement in Neuropathic Pain

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Histamine Modulation of Acute Nociception Involves Regulation of Na_v1.8 in Primary Afferent Neurons in Mice

Histamine Upregulates Nav1.8 Expression in Primary Afferent Neurons via H₂ Receptors: Involvement in Neuropathic Pain