Nav1.7 sodium channel expression in human lingual nerve neuromas

Bird, Emma V.; Robinson, P.P.; Boissonade, Fiona M.

doi:10.1016/j.archoralbio.2006.11.011

Cited by 30 publications

(27 citation statements)

References 36 publications

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“…No labelling was present in tissue sections where primary antibodies for PGP9.5 and the sodium channel subtypes were omitted, as previously described for PGP9.5 [22] and as shown in Figure 1.…”

Section: Resultsmentioning

confidence: 99%

Correlation of Nav1.8 and Nav1.9 Sodium Channel Expression with Neuropathic Pain in Human Subjects with Lingual Nerve Neuromas

et al. 2013

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BackgroundVoltage-gated sodium channels Nav1.8 and Nav1.9 are expressed preferentially in small diameter sensory neurons, and are thought to play a role in the generation of ectopic activity in neuronal cell bodies and/or their axons following peripheral nerve injury. The expression of Nav1.8 and Nav1.9 has been quantified in human lingual nerves that have been previously injured inadvertently during lower third molar removal, and any correlation between the expression of these ion channels and the presence or absence of dysaesthesia investigated.ResultsImmunohistochemical processing and quantitative image analysis revealed that Nav1.8 and Nav1.9 were expressed in human lingual nerve neuromas from patients with or without symptoms of dysaesthesia. The level of Nav1.8 expression was significantly higher in patients reporting pain compared with no pain, and a significant positive correlation was observed between levels of Nav1.8 expression and VAS scores for the symptom of tingling. No significant differences were recorded in the level of expression of Nav1.9 between patients with or without pain.ConclusionsThese results demonstrate that Nav1.8 and Nav1.9 are present in human lingual nerve neuromas, with significant correlations between the level of expression of Nav1.8 and symptoms of pain. These data provide further evidence that changes in expression of Nav1.8 are important in the development and/or maintenance of nerve injury-induced pain, and suggest that Nav1.8 may be a potential therapeutic target.

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Section: Resultsmentioning

confidence: 99%

Correlation of Nav1.8 and Nav1.9 Sodium Channel Expression with Neuropathic Pain in Human Subjects with Lingual Nerve Neuromas

et al. 2013

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“…Nav1.7 protein and current are both increased in the DRG in a rat model of painful diabetic neuropathy [49,50], whereas the amount of Nav1.7 protein is reduced in the injured DRG after SNL, SNI, and sciatic nerve axotomy in animals [25,51]. The level of Nav1.7 protein is also decreased in the injured DRG of humans after peripheral axotomy or traumatic central axotomy [52], but Nav1.7 protein has been observed to accumulate in painful neuromas of amputees with phantom limb pain [29,53]. Interestingly, a mouse behavioral study showed that conditional knockout of DRG Nav1.7 did not affect SNL-induced development of mechanical allodynia [54].…”

Section: Introductionmentioning

confidence: 99%

Are Voltage-Gated Sodium Channels on the Dorsal Root Ganglion Involved in the Development of Neuropathic Pain?

et al. 2011

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Neuropathic pain is a common clinical condition. Current treatments are often inadequate, ineffective, or produce potentially severe adverse effects. Understanding the mechanisms that underlie the development and maintenance of neuropathic pain will be helpful in identifying new therapeutic targets and developing effective strategies for the prevention and/or treatment of this disorder. The genesis of neuropathic pain is reliant, at least in part, on abnormal spontaneous activity within sensory neurons. Therefore, voltage-gated sodium channels, which are essential for the generation and conduction of action potentials, are potential targets for treating neuropathic pain. However, preclinical studies have shown unexpected results because most pain-associated voltage-gated channels in the dorsal root ganglion are down-regulated after peripheral nerve injury. The role of dorsal root ganglion voltage-gated channels in neuropathic pain is still unclear. In this report, we describe the expression and distribution of voltage-gated sodium channels in the dorsal root ganglion. We also review evidence regarding changes in their expression under neuropathic pain conditions and their roles in behavioral responses in a variety of neuropathic pain models. We finally discuss their potential involvement in neuropathic pain.

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“…These can be at multiple sites along the axons, including distal terminals. Evidence from earlier studies has implicated multiple sites in the generation of ectopic activity, including peripheral nerve terminals (Albrecht et al, 2006;Kauppila et al, 2002;Pare et al, 2007), at the site of nerve injury (Bird et al, 2007;Coward et al, 2000;Devor et al, 1993;Novakovic et al, 1998;Omana-Zapata et al, 1997a,b;Tal and Eliav, 1996), along the nerve (Amir et al, 2005;Gold et al, 2003;Pertin et al, 2005), adjacent nerves (Sotgiu et al, 2006), and in the dorsal root ganglia (Amir et al, 1999;Chaplan et al, 2003;Craner et al, 2002;Liu et al, 2000bLiu et al, , 2002Michaelis et al, 2000;Na et al, 2000;Novakovic et al, 1998;Omana-Zapata et al, 1997a,b;Study and Kral, 1996;Xie et al, 1995).…”

Section: Site Of Generation Of Peripheral Drivementioning

confidence: 99%

Governing role of primary afferent drive in increased excitation of spinal nociceptive neurons in a model of sciatic neuropathy

Pitcher

Henry

2008

Experimental Neurology

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Previously we reported that the cuff model of peripheral neuropathy, in which a 2 mm polyethylene tube is implanted around the sciatic nerve, exhibits aspects of neuropathic pain behavior in rats similar to those in humans and causes robust hyperexcitation of spinal nociceptive dorsal horn neurons. The mechanisms mediating this increased excitation are not known and remain a key unresolved question in models of peripheral neuropathy. In anesthetized adult male Sprague-Dawley rats 2-6 weeks after cuff implantation we found that elevated discharge rate of single lumbar (L 3-4 ) wide dynamic range (WDR) neurons persists despite acute spinal transection (T9) but is reversed by local conduction block of the cuff-implanted sciatic nerve; lidocaine applied distal to the cuff (i.e. between the cuff and the cutaneous receptive field) decreased spontaneous baseline discharge of WDR dorsal horn neurons ~40% (n=18) and when applied subsequently proximal to the cuff, i.e. between the cuff and the spinal cord, it further reduced spontaneous discharge by ~60% (n=19; P<0.05 proximal vs. distal) to a level that was not significantly different from that of naive rats. Furthermore, in cuff-implanted rats WDR neurons (n=5) responded to mechanical cutaneous stimulation with an exaggerated afterdischarge which was reversed entirely by proximal nerve conduction block. These results demonstrate that the hyperexcited state of spinal dorsal horn neurons observed in this model of peripheral neuropathy is not maintained by tonic descending facilitatory mechanisms. Rather, on-going afferent discharges originating from the sciatic nerve distal to, at, and proximal to the cuff maintain the synapticallymediated gain in discharge of spinal dorsal horn WDR neurons and hyperresponsiveness of these neurons to cutaneous stimulation. Our findings reveal that ectopic afferent activity from multiple regions along peripheral nerves may drive CNS changes and the symptoms of pain associated with peripheral neuropathy.

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Nav1.7 sodium channel expression in human lingual nerve neuromas

Cited by 30 publications

References 36 publications

Correlation of Nav1.8 and Nav1.9 Sodium Channel Expression with Neuropathic Pain in Human Subjects with Lingual Nerve Neuromas

Correlation of Nav1.8 and Nav1.9 Sodium Channel Expression with Neuropathic Pain in Human Subjects with Lingual Nerve Neuromas

Are Voltage-Gated Sodium Channels on the Dorsal Root Ganglion Involved in the Development of Neuropathic Pain?

Governing role of primary afferent drive in increased excitation of spinal nociceptive neurons in a model of sciatic neuropathy

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