ArticleThe Journal of physiology2009
Activation of neurokinin 3 receptor increases Na(v)1.9 current in enteric neurons.
Article in The Journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 42 citations in OpenAlex.
- Tachykinin signaling defines distinct populations of glia in the enteric nervous system.Neuron · 2026Article
- The influence of Nav1.9 channels on intestinal hyperpathia and dysmotility.Channels (Austin, Tex.) · 2023Review
- Impaired cecal motility and secretion alongside expansion of gut-associated lymphoid tissue in the Nlgn3Scientific reports · 2023Article
- Tachykinin receptor 3 in the lateral habenula alleviates pain and anxiety comorbidity in mice.Frontiers in immunology · 2023Article
- NaJournal of neurophysiology · 2022Article
- Estrogen-dependent depressor response of melatonin via baroreflex afferent function and intensification of PKC-mediated NaActa pharmacologica Sinica · 2022Article
- The development of somatosensory neurons: Insights into pain and itch.Current topics in developmental biology · 2021Review
- Voltage-gated sodium channels: (NaThe Journal of physiology · 2018Review
- Cholera Toxin Induces Sustained Hyperexcitability in Myenteric, but Not Submucosal, AH Neurons in Guinea Pig Jejunum.Frontiers in physiology · 2017Article
- NaV1.9: a sodium channel linked to human pain.Nature reviews. Neuroscience · 2015Review
- The role of sodium channels in painful diabetic and idiopathic neuropathy.Current diabetes reports · 2014Review
- Specialized functions of Nav1.5 and Nav1.9 channels in electrogenesis of myenteric neurons in intact mouse ganglia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Nicotine enhances excitability of medial habenular neurons via facilitation of neurokinin signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- A de novo gain-of-function mutation in SCN11A causes loss of pain perception.Nature genetics · 2013Article
- Electrophysiological characteristics of enteric neurons isolated from the immortomouse.Digestive diseases and sciences · 2013Article
- The Nav1.9 channel regulates colonic motility in mice.Frontiers in neuroscience · 2013Article
- Novel functional roles for enteric glia in the gastrointestinal tract.Nature reviews. Gastroenterology & hepatology · 2012Review
- Review
- Functional properties and toxin pharmacology of a dorsal root ganglion sodium channel viewed through its voltage sensors.The Journal of general physiology · 2011Article
- Patch clamp recording from enteric neurons in situ.Nature protocols · 2011Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The intrinsic primary afferent neurons (IPANs) of the guinea pig enteric nervous system express Na(v)1.9 sodium channels that produce a persistent TTX-resistant current having a low activation threshold and slow gating kinetics. These neurons receive slow EPSPs induced mainly by the activation of neurokinin 3 receptors (NK3r). Here, we demonstrate that senktide, a specific NK3r agonist, potentiates the Na(v)1.9 current (I(Nav1.9)) in IPANs. Using whole-cell patch-clamp recordings from IPANs in duodenum longitudinal muscle/myenteric plexus preparations, we show that short (1-5 s) and long (up to 1 min) applications of senktide, increase the I(Nav1.9) peak current up to 13-fold. The effect, blocked by a NK3r antagonist SB235375 is transient, lasting approximately 2 min and is due to a negative shift of the activation voltage by approximately 20 mV and of fast inactivation by approximately 10 mV. As a consequence, the window current resulting from the product of the activation and fast inactivation curves is shifted and enlarged. The transient effect of senktide is likely to be due to the fast desensitization of NK3r. Protein kinase C (PKC) activation with phorbol or oleoyl acetylglycerol also increases I(Nav1.9), although persistently, by inducing similar voltage-dependent changes. Current-clamp experiments showed that I(Nav1.9) modulation by senktide lowers action potential threshold and increases excitability. The increase in I(Nav1.9) by NK3r activation is also likely to amplify slow EPSPs generated in the IPANs. These changes in excitability potentially have a profound effect on the entire enteric synaptic circuit and ultimately on gut motility and secretion.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.