Phenotypes and peripheral mechanisms underlying inflammatory pain-related behaviors induced by BmK I, a modulator of sodium channels

Bai, Zhan-Tao; Liu, Tong; Jiang, Feng; Cheng, Ming; Pang, Xiaowu; Hua, Liming; Shi, Jing; Zhou, Jingjing; Shu, Xueqin; Zhang, Jianwei; Ji, Yonghua

doi:10.1016/j.expneurol.2010.08.018

Cited by 24 publications

(30 citation statements)

References 52 publications

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“…There is still no induced by BmK I in rats. The mechanosensitivity peaked at 2-8 h after BmK I administration [26] . As activated mTOR promotes functional protein synthesis, based on the gatecontrol theory of pain, we suppose that mTOR activated in the contralateral DRG might contribute to the synthesis of proteins and peptides associated with mechanosensitivity.…”

Section: Scorpion Sting Stimulated the Mtor Signaling Pathway In Drgmentioning

confidence: 96%

“…BmK I, a toxin specific to VGSC receptor site 3, increases Na + currents and delays the inactivation of VGSCs [26] . Intraplantar (i.pl.)…”

Section: Variousmentioning

confidence: 99%

“…injection of BmK I induces many pain responses in rats, such as spontaneous reflexes, paroxysmal pain-like behaviors, thermal hypersensitivity, and bilateral (mirror-image) mechanical hypersensitivity [26] . It is therefore considered to be the main contributor to scorpion envenomationinduced pain [26,27] . Compared to other animal models of pain, the BmK I model has a unique mechanism.…”

Section: Variousmentioning

confidence: 99%

“…Compared to other animal models of pain, the BmK I model has a unique mechanism. Our previous studies showed that the dynamic modulation by BmK I of Na + channels on peripheral primary afferent fi bers, especially capsaicin-sensitive fi bers, contributes to pain sensation [26,28] . The pain of a scorpion sting is, at least partly, due to peripheral nerve sensitization.…”

Section: Variousmentioning

confidence: 99%

“…The measurement of spontaneous nociceptive responses and paw withdrawal mechanical threshold (PWMT) followed the methods described by Bai et al [26] . Briefl y, the …”

Section: Behavioral Testsmentioning

confidence: 99%

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Activation of mammalian target of rapamycin contributes to pain nociception induced in rats by BmK I, a sodium channel-specific modulator

et al. 2013

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Section: Scorpion Sting Stimulated the Mtor Signaling Pathway In Drgmentioning

confidence: 96%

“…BmK I, a toxin specific to VGSC receptor site 3, increases Na + currents and delays the inactivation of VGSCs [26] . Intraplantar (i.pl.)…”

Section: Variousmentioning

confidence: 99%

Section: Variousmentioning

confidence: 99%

Section: Variousmentioning

confidence: 99%

“…The measurement of spontaneous nociceptive responses and paw withdrawal mechanical threshold (PWMT) followed the methods described by Bai et al [26] . Briefl y, the …”

Section: Behavioral Testsmentioning

confidence: 99%

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Activation of mammalian target of rapamycin contributes to pain nociception induced in rats by BmK I, a sodium channel-specific modulator

et al. 2013

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Chemical and Biological Tools for the Study of Voltage‐Gated Sodium Channels in Electrogenesis and Nociception

Elleman

Bois

2022

ChemBioChem

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The malfunction and misregulation of voltage‐gated sodium channels (NaVs) underlie in large part the electrical hyperexcitability characteristic of chronic inflammatory and neuropathic pain. NaVs are responsible for the initiation and propagation of electrical impulses (action potentials) in cells. Tissue and nerve injury alter the expression and localization of multiple NaV isoforms, including NaV1.1, 1.3, and 1.6–1.9, resulting in aberrant action potential firing patterns. To better understand the role of NaV regulation, localization, and trafficking in electrogenesis and pain pathogenesis, a number of chemical and biological reagents for interrogating NaV function have been advanced. The development and application of such tools for understanding NaV physiology are the focus of this review.

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Scorpion Venoms

2015

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In recent years, the field of toxinology has expanded substantially. On the one hand it studies venomous animals, plants and micro organisms in detail to understand their mode of action on targets. While on the other, it explores the biochemical composition, genomics and proteomics of toxins and venoms to understand their three interaction with life forms (especially humans), development of antidotes and exploring their pharmacological potential. Therefore, toxinology has deep linkages with biochemistry, molecular biology, anatomy and pharmacology. In addition, there is a fast-developing applied subfield, clinical toxinology, which deals with understanding and managing medical effects of toxins on human body. Given the huge impact of toxin-based deaths globally, and the potential of venom in generation of drugs for so-far incurable diseases (for example, diabetes, chronic pain), the continued research and growth of the field is imminent. This has led to the growth of research in the area and the consequent scholarly output by way of publications in journals and books. Despite this ever-growing body of literature within biomedical sciences, there is still no all-inclusive reference work available that collects all of the important biochemical, biomedical and clinical insights relating to toxinology. Composed of 11 volumes, Toxinology provides comprehensive and authoritative coverage of the main areas in toxinology, from fundamental concepts to new developments and applications in the field. Each volume comprises a focused and carefully chosen collection of contributions from leading names in the subject.

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Phenotypes and peripheral mechanisms underlying inflammatory pain-related behaviors induced by BmK I, a modulator of sodium channels

Cited by 24 publications

References 52 publications

Activation of mammalian target of rapamycin contributes to pain nociception induced in rats by BmK I, a sodium channel-specific modulator

Activation of mammalian target of rapamycin contributes to pain nociception induced in rats by BmK I, a sodium channel-specific modulator

Chemical and Biological Tools for the Study of Voltage‐Gated Sodium Channels in Electrogenesis and Nociception

Scorpion Venoms

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