• Corpus ID: 14658801

Experimental and computational evidence for an essential role of 1 NaV 1 . 6 in spike initiation at stretch-sensitive colorectal afferent 2 endings 3

@inproceedings{Feng2015ExperimentalAC,
  title={Experimental and computational evidence for an essential role of 1 NaV 1 . 6 in spike initiation at stretch-sensitive colorectal afferent 2 endings 3},
  author={Bin Feng and Yi Zhu and Jun-Ho La and Zachary P. Wills and Gerald F. Gebhart},
  year={2015}
}
Experimental and computational evidence for an essential role of 1 NaV1.6 in spike initiation at stretch-sensitive colorectal afferent 2 endings 3 Bin Feng, Yi Zhu, Jun-Ho La, Zachary P. Wills, and G.F. Gebhart 4 Center for Pain Research, Department of Anesthesiology and Department of 5 Neurobiology, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, 6 USA 7 Abbreviated title: NaV1.6 in spike initiation of colorectal afferents 8 Manuscript length: 49 pages, 9 figures, 4 tables… 

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References

SHOWING 1-10 OF 70 REFERENCES

μ-Conotoxins that differentially block sodium channels NaV1.1 through 1.8 identify those responsible for action potentials in sciatic nerve

TLDR
This is the first report describing a qualitative pharmacological survey of TTX-sensitive NaV1 isoforms responsible for propagating action potentials in peripheral nerve, and a panel of μ-conopeptides should be useful in identifying the functional contributions of NaV 1 isoforms in other preparations.

Simulation in sensory neurons reveals a key role for delayed Na+ current in subthreshold oscillations and ectopic discharge: implications for neuropathic pain.

TLDR
The use of a more complete set of Na+ conductances--which includes several delayed components--enables simulation of the entire repertoire of oscillation-triggered electrogenic phenomena seen in live dorsal root ganglion neurons, revealing the key conductances that underlie afferent ectopia.

Dissecting the role of sodium currents in visceral sensory neurons in a model of chronic hyperexcitability using Nav1.8 and Nav1.9 null mice

TLDR
A critical role is identified forNav1.8 in chronic post‐infectious visceral hyperexcitability, with no contribution from Nav1.9.

ProTx-II, a Selective Inhibitor of NaV1.7 Sodium Channels, Blocks Action Potential Propagation in Nociceptors

TLDR
The 125I-ProTx-II binding assay, described here, offers a new tool in the search for novel NaV1.7-selective channel blockers, suggesting that ProTx- II binds to a novel site, which may be more conducive to conferring subtype selectivity than the site occupied by traditional local anesthetics and anticonvulsants.

Distinct contributions of Nav1.6 and Nav1.2 in action potential initiation and backpropagation

TLDR
Modeling studies and simultaneous somatic and axonal recordings showed that distal Nav1.6 promotes action potential initiation, whereas proximal Nav 1.2 promotes its backpropagation to the soma.

Small-Fiber Neuropathy Nav1.8 Mutation Shifts Activation to Hyperpolarized Potentials and Increases Excitability of Dorsal Root Ganglion Neurons

TLDR
Observations suggest that the effects of this mutation on activation and ramp current are dominant over the reduced persistent current, and show that these pro-excitatory gating changes confer hyperexcitability on peripheral sensory neurons, which may contribute to pain in this individual with painful I-SFN.

Two TTX-resistant Na+ currents in mouse colonic dorsal root ganglia neurons and their role in colitis-induced hyperexcitability.

TLDR
It is suggested that colitis alters trkA-positive neurons to preferentially increase slow TTX-R Na+ (Nav1.8) Na+ current, which is associated with increased slow TTx-R (Nav 1.8), which is implicated in inflammatory pain.

Differences in spinal distribution and neurochemical phenotype of colonic afferents in mouse and rat

TLDR
The high incidence of TRPV1‐positive colonic afferents in rodents suggests that hypersensitivity from the viscera may be partially a TRPv1‐mediated event, thereby providing a suitable target for the treatment of visceral pain.

Extra spike formation in sensory neurons and the disruption of afferent spike patterning.

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