Expression and localization of the Nav1.9 sodium channel in enteric neurons and in trigeminal sensory endings: Implication for intestinal reflex function and orofacial pain

Padilla, Françoise; Couble, Marie‐Lise; Coste, Bertrand; Maingret, François; Clerc, Nadine; Crest, Marcel; Ritter, Amy M.; Magloire, H.; Delmas, Patrick

doi:10.1016/j.mcn.2007.02.008

Cited by 74 publications

(72 citation statements)

References 71 publications

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“…An increase in channel expression, or a left shift in the activation curve in TTX-R currents, could also explain the increased excitability and decreased threshold we recorded since these currents not only modify the readiness with which an action potential is evoked but also influence subthreshold membrane oscillations near threshold (7,8,30).…”

Section: Discussionmentioning

confidence: 92%

Lactobacillus reuteri ingestion prevents hyperexcitability of colonic DRG neurons induced by noxious stimuli

Ma¹,

Mao²,

Wang³

et al. 2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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Kunze W. Lactobacillus reuteri ingestion prevents hyperexcitability of colonic DRG neurons induced by noxious stimuli. Am J Physiol Gastrointest Liver Physiol 296: G868 -G875, 2009. First published January 29, 2009 doi:10.1152/ajpgi.90511.2008.-Lactobacillus species ingestion can decrease autonomic responses and spinal fiber discharge to nociceptive colorectal distension (CRD), even in the absence of inflammation. The present study aimed to determine whether dorsal root ganglion (DRG) somas could be a locus where the antinociceptive probiotic may have an effect. Healthy rats were fed with Lactobacillus reuteri or vehicle control for 9 days whereupon they were anesthetized, and intermittent distal colonic CRD at 80 mmHg distension was either performed for 1 h or not. The animals were immediately euthanized and patch-clamp recordings taken after isolation and overnight culture from those DRG that projected to the distal colon. CRD decreased the threshold for action potential generation and increased the number of spikes discharged during a standard depolarizing test stimulus, and this effect was blocked by prior probiotic ingestion. The increase in excitability was paralleled by an increase in DRG capacitance, which was not altered by Lactobacillus reuteri ingestion. CRD did not increase tissue weight or myeloperoxidase activity. We suggest that the effects of CRD may have been caused by activity-dependent neurotransmission between DRG somas. CRD evoked increases in action potential upstroke speed, which suggests that it may also have led to augmentation of sodium channel conductances. Probiotic ingestion may have interfered with this hypothetical mechanism since it blocked the effect of CRD on the action potential. colorectal distension; dorsal root ganglion; probiotics; sensory neurons PROBIOTICS ARE HEALTH-PROMOTING commensal bacteria that can have therapeutic or preventative roles when ingested. Probiotics are most frequently of the Lactobacillus or Bifidobacterium species, and clinically beneficial effects of probiotics have been described in travelers' diarrhea, irritable bowel syndrome, and inflammatory bowel disease (13,29,35,44,46). In addition, probiotics can modulate postinflammatory gut hypersensitivity and alter neuropeptide content (20,43). Because of their therapeutic potential and their presumed consumer safety, the actions of probiotics on the physiological mechanisms underlying peripheral and centrally directed nociceptive signals are increasingly being investigated.Ingestion of probiotic commensals can decrease colorectal distension (CRD)-evoked pain in healthy animals, that is, in the absence of overt inflammation in the intestine. Experimental modulation of intestinal motility (32) and visceral pain (18,32,43) by Lactobacillus species have been convincingly demonstrated for the murine colon. Lactobacillus reuteri (L. reuteri) ingestion can alter the excitability of myenteric intrinsic sensory neurons that were recorded from colon segments taken from healthy rats. Remarkably, in anesthetized he...

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Section: Discussionmentioning

confidence: 92%

Lactobacillus reuteri ingestion prevents hyperexcitability of colonic DRG neurons induced by noxious stimuli

Ma¹,

Mao²,

Wang³

et al. 2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Tetrodotoxin (TTX) is a neurotoxin, which inhibits voltage-dependent Na + currents in many neurones (Catterall 1980), although tetrodotoxin-resistant Na + channels are known, too (see e.g. Browning and Lees 1996, Padilla et al 2007). …”

Section: Results 51mentioning

confidence: 99%

“…Although action potentials in AH-neurones have been found to be generated by TTX-sensitive Na + currents and by N-type high voltage-activated (HVA) Ca 2+ channels (Rugiero et al 2002), it has also been shown by the same author (Rugiero et al 2002) that this sensitivity to TTX is quite poor as they had to use very high TTX concentrations (ranging from 500 nmol/l up to 2 µmol/l). In addition, tetrodotoxin-resistant Na + channels of the type Nav1.9 are expressed by a subpopulation of myenteric neurones, which, however, due to their slow gating properties, are thought to contribute predominantly to the amplification of slow excitatory postsynaptic potentials at the neuronal soma (Padilla et al 2007). …”

Section: Alteration Of the Excitabilitymentioning

confidence: 99%

Effects of H2O2 at rat myenteric neurones in culture

Pouokam

Rehn

Diener

2009

European Journal of Pharmacology

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“…La sous-unité Nav1.9 est observée majoritairement dans les neurones de petit diamètre des ganglions rachidiens et trigéminaux et plus sporadiquement dans les neurones de moyen diamètre. Cette sous-unité est également présente au niveau des terminaisons libres et des zones réceptives des fibres sensitives de la peau des lèvres et de la pulpe dentaire [62]. Le courant Nav1.9 est un courant sodium atypique dans la mesure où il possède un seuil d'activation relativement négatif et des cinétiques d'activation et d'inactivation extrêmement lentes [20,21] (Fig.…”

Section: Canaux Sodium Des Neurones Sensorielsunclassified

“…Activation des courants Nav1.9 (en jaune) et Nav1.8 (en rouge) dans des neurones nociceptifs en réponse à des créneaux de potentiel. Ces courants aux cinétiques lentes sont des marqueurs des neurones nociceptifs [20,21,58,62] Rôle des différentes sous-unités Sous-unités Nav1.1 et Nav1.6…”

Section: Implication Dans Les Décharges Ectopiques Spontanéesunclassified

Rôle des canaux sodium des neurones afférents primaires dans les douleurs neuropathiques périphériques

Maingret

Delmas

2008

Douleur analg

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Management of neuropathic pain remains a major clinical challenge. Clinical and experimental data indicate that changes in the expression of voltage-gated sodium channels play a key role in the pathogenesis of neuropathic pain. Several of the sodium channel isoforms that are implicated in neuropathic pain states are selectively expressed in somatosensory primary afferent neurons. This restricted expression pattern raises the possibility that isoform-specific drugs might be analgesic and lack the cardiotoxicity and neurotoxicity that limit the use of current sodium channel blockers.

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Expression and localization of the Nav1.9 sodium channel in enteric neurons and in trigeminal sensory endings: Implication for intestinal reflex function and orofacial pain

Cited by 74 publications

References 71 publications

Lactobacillus reuteri ingestion prevents hyperexcitability of colonic DRG neurons induced by noxious stimuli

Lactobacillus reuteri ingestion prevents hyperexcitability of colonic DRG neurons induced by noxious stimuli

Effects of H2O2 at rat myenteric neurones in culture

Rôle des canaux sodium des neurones afférents primaires dans les douleurs neuropathiques périphériques

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