Behavioural and histological observations of sensory impairment caused by tight ligation of the trigeminal nerve in mice

Seino, Hiroyuki; Seo, Kenji; Maeda, Takeyasu; Someya, Genji

doi:10.1016/j.jneumeth.2009.04.020

Cited by 24 publications

(17 citation statements)

References 24 publications

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“…Similar functional outcome is reported with partial transection of the infraorbital nerve in another study [6]. In another previous report, sensation impairment persists more than 10 weeks after tight ligation of the mental nerve in mice, however, the behavioral test describes grabbing the mice from the back to take pain threshold measurements in this unnatural posture [7]. …”

Section: Introductionsupporting

confidence: 77%

Orofacial neuropathic pain mouse model induced by Trigeminal Inflammatory Compression (TIC) of the infraorbital nerve

Zhang

Lyons

et al. 2012

Mol Brain

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BackgroundTrigeminal neuropathic pain attacks can be excruciating for patients, even after being lightly touched. Although there are rodent trigeminal nerve research models to study orofacial pain, few models have been applied to studies in mice. A mouse trigeminal inflammatory compression (TIC) model is introduced here which successfully and reliably promotes vibrissal whisker pad hypersensitivity.ResultsThe chronic orofacial neuropathic pain model is induced after surgical placement of chromic gut suture in the infraorbital nerve fissure in the maxillary bone. Slight compression and chemical effects of the chromic gut suture on the portion of the infraorbital nerve contacted cause mild nerve trauma. Nerve edema is observed in the contacting infraorbital nerve bundle as well as macrophage infiltration in the trigeminal ganglia. Centrally in the spinal trigeminal nucleus, increased immunoreactivity for an activated microglial marker is evident (OX42, postoperative day 70). Mechanical thresholds of the affected whisker pad are significantly decreased on day 3 after chromic gut suture placement, persisting at least 10 weeks. The mechanical allodynia is reversed by suppression of microglial activation. Cold allodynia was detected at 4 weeks.ConclusionsA simple, effective, and reproducible chronic mouse model mimicking clinical orofacial neuropathic pain (Type 2) is induced by placing chromic gut suture between the infraorbital nerve and the maxillary bone. The method produces mild inflammatory compression with significant continuous mechanical allodynia persisting at least 10 weeks and cold allodynia measureable at 4 weeks.

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Section: Introductionsupporting

confidence: 77%

Orofacial neuropathic pain mouse model induced by Trigeminal Inflammatory Compression (TIC) of the infraorbital nerve

Zhang

Lyons

et al. 2012

Mol Brain

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“…Studies by Marinković et al [18] indicated that SP expression was increased in the branch of the trigeminal nerve removed from a patient with TN. Other studies on the animal model of TN also demonstrated the increased SP and NK1 in the trigeminal nerve or brain tissues [19,20] .…”

Section: Discussionmentioning

confidence: 83%

Analgesic effect of diprospan in rats with trigeminal neuralgia

Wang

Cao

et al. 2011

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

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This study examined the analgesic effect of diprospan in rats with trigeminal neuralgia. Rat model of trigeminal neuralgic pain was established by loosely ligating the left infraorbital branch of the trigeminal nerve. After allodynia developed, the rats were randomly divided into 2 groups (n=20 in each): diprospan group, in which the rats received diprospan (7 mg/mL, 0.1 mL) injected to the left infraorbital foramen area; control group, in which saline (0.1 mL) was administered as the same manner as the diprospan group. The pain threshold (PT) in the left infraorbital area was measured before and 2, 6, and 8 weeks after the administration. The expression of neuropeptides [substance P, preprotachykinin A (PPTA), calcitonin gene-related peptide (CGRP)] in the trigeminal nerve was detected at the same time points as the PT measurement by immunohistochemistry or in situ hybridization method. The results showed that in the diprospan group, the PT was 10.65 ± 1.26, 10.77 ± 1.19 and 14.13 ± 1.34 g 2, 6, and 8 weeks after the administration respectively, significantly higher than that before the administration (PT value: 0.36 ± 0.11) (P<0.05 for each). In the saline group, the PT was 0.37 ± 0.13, 0.66 ± 0.09, 4.45 ± 1.29 and 13.72 ± 1.72 g before and 2, 6, and 8 weeks after the administration respectively with differences being significant between before and 6, 8 weeks after the administration (P<0.01). No significant difference existed in the PT between the diprospan group and the saline group at pre-administration (P>0.05). The PT in the diprospan group was significantly greater than that in the saline group 2 and 6 weeks post-administration (P<0.05). In the diprospan group, the expression levels of neuropeptides were significantly reduced as compared with those in the saline group 2 and 6 weeks post-administration (P<0.05). It was concluded that diprospan has an obvious analgesic effect on the trigeminal neuropathic pain partly by reducing the expression of neuropeptides in the trigeminal ganglia.

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“…To reduce any effects of restraint, either by hand (Seino et al, 2009) or grasping the tail (Krzyzanowska et al, 2011), on behavioral assessment of the mice, we adopted a less stressful method (Aita et al, 2010) and developed a more precise probing technique to test mechanical hypersensitivity in V2 and V3 skin. Mice were placed in a box (3×3×4 inch) with the top, bottom and four walls made of black wire mesh and allowed to freely move.…”

Section: Methodsmentioning

confidence: 99%

Central Terminal Sensitization of TRPV1 by Descending Serotonergic Facilitation Modulates Chronic Pain

Kim

Chu

Han

et al. 2014

Neuron

280

273

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SUMMARY The peripheral terminals of primary nociceptive neurons play an essential role in pain detection mediated by membrane receptors like TRPV1, a molecular sensor of heat and capsaicin. However, the contribution of central terminal TRPV1 in the dorsal horn to chronic pain has not been investigated directly. Combining primary sensory neuron-specific GCaMP3 imaging with a trigeminal neuropathic pain model, we detected robust neuronal hyperactivity in injured and uninjured nerves in the skin, soma in trigeminal ganglion, and central terminals in the spinal trigeminal nucleus. Extensive TRPV1 hyperactivity was observed in central terminals innervating all dorsal horn laminae. The central terminal TRPV1 sensitization was maintained by descending serotonergic (5-HT) input from the brainstem. Central blockade of TRPV1 or 5-HT/5-HT3A receptors attenuated central terminal sensitization, excitatory primary afferent inputs, and mechanical hyperalgesia in the territories of injured and uninjured nerves. Our results reveal new central mechanisms facilitating central terminal sensitization underlying chronic pain.

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Behavioural and histological observations of sensory impairment caused by tight ligation of the trigeminal nerve in mice

Cited by 24 publications

References 24 publications

Orofacial neuropathic pain mouse model induced by Trigeminal Inflammatory Compression (TIC) of the infraorbital nerve

Orofacial neuropathic pain mouse model induced by Trigeminal Inflammatory Compression (TIC) of the infraorbital nerve

Analgesic effect of diprospan in rats with trigeminal neuralgia

Central Terminal Sensitization of TRPV1 by Descending Serotonergic Facilitation Modulates Chronic Pain

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