The role of large-conductance, calcium-activated potassium channels in a rat model of trigeminal neuropathic pain

Liu, Caiyue; Lu, Zhan-ying; Li, Na; Yu, Liqing; Zhao, Yirong; Ma, Baohua

doi:10.1177/0333102414534083

Cited by 42 publications

(39 citation statements)

References 73 publications

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“…In our model, enhanced asymmetric face-grooming was observed in dIoN-CCI rats over a prolonged period of time. In contrast, the nociceptive behavior of rats subjected to previous IoN-CCI procedures varies depending on the specific type of procedure used in different studies 6, 13, 16, 17 . Some studies showed that IoN-CCI rats exhibited an early phase hyposensitivity and a late phase hypersensitivity to mechanical stimulation in the IoN territory 13, 25 .…”

Section: Discussionmentioning

confidence: 99%

An Improved Rodent Model of Trigeminal Neuropathic Pain by Unilateral Chronic Constriction Injury of Distal Infraorbital Nerve

Ding

You

Shen

et al. 2017

The Journal of Pain

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The number of studies on trigeminal nerve injury using animal models remains limited. A rodent model of trigeminal neuropathic pain was first developed in the 1994, in which chronic constriction injury is induced by ligation of the infraorbital nerve (IoN-CCI). This animal model has served as a major tool to study trigeminal neuropathic pain. Unfortunately, the surgical procedure in this model is complicated and far more difficult than ligation of peripheral nerves (e.g. sciatic nerve). The aim of this study was to improve on the current surgical procedure of IoN ligation to induce trigeminal neuropathic pain in rats. We demonstrate that the IoN can be readily accessed through a small facial incision. Chronic constriction injury can be induced by ligation of a segment at the distal infraorbital nerve (dIoN-CCI). This dIoN-CCI procedure is simple, minimally invasive and time-saving. Our data show that the dIoN-CCI procedure consistently induced both acute and chronic nociceptive behaviors in rats. Daily gabapentin treatment attenuated mechanical allodynia and reduced face-grooming episodes in dIoN-CCI rats. Perspective The orofacial pain caused by trigeminal nerve damage is severe and perhaps more debilitating than other types of neuropathic pain. However, studies on trigeminal neuropathic pain remain limited. This is largely due to the lack of proper animal models given the complexity of the existing surgical procedure required to induce trigeminal nerve injury. Our improved dIoN-CCI model is likely to make it more accessible to study the cellular and molecular mechanisms of neuropathic pain caused by trigeminal nerve damage.

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Section: Discussionmentioning

confidence: 99%

An Improved Rodent Model of Trigeminal Neuropathic Pain by Unilateral Chronic Constriction Injury of Distal Infraorbital Nerve

Ding

You

Shen

et al. 2017

The Journal of Pain

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“…This multifunctionality can be an optimal strategy for the construction of biologically active peptides allowing sea anemones to be active predators through the production of neurotoxins and resist bacterial infections caused by the eventual injury of the tentacles. It is noteworthy that human β-defensin 2 (Hbd-2), the structural homologue of Ueq 12-1, possess antimicrobial properties, act as an opener of large-conductance Ca 2+ -activated potassium (BKCa)-mSlo+hβ1 channels and inhibit Kv1.3-channels [38,51,52]. These studies highlight the multifunctionality observed for this particular spatial fold.…”

Section: Discussionmentioning

confidence: 99%

New Disulfide-Stabilized Fold Provides Sea Anemone Peptide to Exhibit Both Antimicrobial and TRPA1 Potentiating Properties

Logashina

Solstad

Mineev

et al. 2017

Toxins

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A novel bioactive peptide named τ-AnmTx Ueq 12-1 (short name Ueq 12-1) was isolated and characterized from the sea anemone Urticina eques. Ueq 12-1 is unique among the variety of known sea anemone peptides in terms of its primary and spatial structure. It consists of 45 amino acids including 10 cysteine residues with an unusual distribution and represents a new group of sea anemone peptides. The 3D structure of Ueq 12-1, determined by NMR spectroscopy, represents a new disulfide-stabilized fold partly similar to the defensin-like fold. Ueq 12-1 showed the dual activity of both a moderate antibacterial activity against Gram-positive bacteria and a potentiating activity on the transient receptor potential ankyrin 1 (TRPA1). Ueq 12-1 is a unique peptide potentiator of the TRPA1 receptor that produces analgesic and anti-inflammatory effects in vivo. The antinociceptive properties allow us to consider Ueq 12-1 as a potential analgesic drug lead with antibacterial properties.

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“…Involvement of ERK and c-fos after estrogen replacement in ovariectomized CFA rats ERK is one member of the mitogen-activated protein kinase (MAPK) family, which is known to have different functions in sensory processing [33][34][35]. In the present study, the expressions of ERKand c-fosin the sham, OVX, and estrogen-treated CFArats were investigated.…”

Section: Estrogen Replacement Reversed the Decrease Of Pwt In Ovariecmentioning

confidence: 92%

Inhibitory effect of estrogen receptor beta on P2X3 receptors during inflammation in rats

Jiang

Sun

et al. 2016

Purinergic Signalling

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Estrogen receptor beta (ERβ) has been shown to play a therapeutic role in inflammatory bowel disease (IBD). However, the mechanism underlying how ERβ exerts therapeutic effects and its relationship with P2X3 receptors (P2X3R) in rats with inflammation is not known. In our study, animal behavior tests, visceromotor reflex recording, and Western blotting were used to determine whether the therapeutic effect of ERβ in rats with inflammation was related with P2X3R. In complete Freund adjuvant (CFA)-induced chronic inflammation in rats, paw withdrawal threshold was significantly decreased which were then reversed by systemic injection of ERβ agonists, DPN or ERB-041. In 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in rats, weight loss, higher DAI scores, increased visceromotor responses, and inflammatory responses were reversed by application of DPN or ERB-041. The higher expressions of P2X3R in dorsal root ganglia (DRG) of CFA-treated rats and those in rectocolon and DRG of TNBS-treated rats were all decreased by injection of DPN or ERB-041. DPN application also inhibited P2X3R-evoked inward currents in DRG neurons from TNBS rats. Mechanical hyperalgesia and increased P2X3 expression in ovariectomized (OVX) CFA-treated rats were reversed by estrogen replacements. Furthermore, the expressions of extracellular signal-regulated kinase (ERK) in DRG and spinal cord dorsal horn (SCDH) and c-fos in SCDH were significantly decreased after estrogen replacement compared with those of OVX rats. The ERK antagonist U0126 significantly reversed mechanical hyperalgesia in the OVX rats. These results suggest that estrogen may play an important therapeutic role in inflammation through downregulation of P2X3R in peripheral tissues and the nervous system, probably via ERβ, suggesting a novel therapeutic strategy for clinical treatment of inflammation.

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The role of large-conductance, calcium-activated potassium channels in a rat model of trigeminal neuropathic pain

Abstract: Our results indicate the important involvement of mainly ERK and p38 MAPK pathways in modulating BKCa channels in ION-CCI TG neurons. BKCa channels represent a new therapeutic target for the clinical treatment of trigeminal neuropathic pain.

Cited by 42 publications

References 73 publications

An Improved Rodent Model of Trigeminal Neuropathic Pain by Unilateral Chronic Constriction Injury of Distal Infraorbital Nerve

An Improved Rodent Model of Trigeminal Neuropathic Pain by Unilateral Chronic Constriction Injury of Distal Infraorbital Nerve

New Disulfide-Stabilized Fold Provides Sea Anemone Peptide to Exhibit Both Antimicrobial and TRPA1 Potentiating Properties

Inhibitory effect of estrogen receptor beta on P2X3 receptors during inflammation in rats

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