NaV1.7 and pain: contribution of peripheral nerves

@article{Hoffmann2018NaV17AP,
  title={NaV1.7 and pain: contribution of peripheral nerves},
  author={Tal Hoffmann and Ohad Sharon and Jürgen Wittmann and Richard W Carr and Alina Vyshnevska and Roberto de Col and Mohammed A. Nassar and Peter W. Reeh and Christian Weidner},
  journal={PAIN},
  year={2018},
  volume={159},
  pages={496–506}
}
Abstract The sodium channel NaV1.7 contributes to action potential (AP) generation and propagation. Loss-of-function mutations in patients lead to congenital indifference to pain, though it remains unclear where on the way from sensory terminals to central nervous system the signalling is disrupted. We confirm that conditional deletion of NaV1.7 in advillin-expressing sensory neurons leads to impaired heat and mechanical nociception in behavioural tests. With single-fiber recordings from… 
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Defining the Functional Role of NaV1.7 in Human Nociception
The physiological function of different voltage-gated sodium channels in pain.
TLDR
The contribution of individual channel subtypes in three key physiological processes necessary for transmission of sensory information to the CNS: transduction of stimuli at peripheral nerve terminals, axonal transmission of action potentials and neurotransmitter release from central terminals are reviewed.
Overexpressed NaV1.7 Channels Confer Hyperexcitability to in vitro Trigeminal Sensory Neurons of CaV2.1 Mutant Hemiplegic Migraine Mice
TLDR
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TLDR
It is found that both the opioid receptor antagonist naloxone and cannabinoid receptor blockers SR141716A (rimonabant) and SR144528 fail to restore acute pain sensitivity in Nav1.7 loss-of-function rats, and this data suggest that endogenous opioid and cannabinoid systems are not required for insensitivity to pain in the absence of Nav 1.7 channels.
NGF-Induced Nav1.7 Upregulation Contributes to Chronic Post-surgical Pain by Activating SGK1-Dependent Nedd4-2 Phosphorylation.
TLDR
Investigating the involvement of Nav1.7 in NGF-induced pain and its role in the maintenance of pain behavior during long-term observations suggests that the maintained upregulation of Nav 1.7 triggered by NGF contributes to the development of CPSP.
Adult‐onset hypothyroidism causes mechanical hypersensitivity due to peripheral nerve hyperexcitability based on voltage‐gated potassium channel downregulation in male mice
TLDR
Fluticasone, which is the anti‐inflammatory agent with an ability to activate the voltage‐gated potassium channel subfamily A (Kv1), restored the decrease in the latency change ratio by PTU exposure under the train‐pulse stimulation supporting the hypothesis that Kv1 may be involved in the conductivity change.
The mechanism of analgesia in NaV1.7 null mutants
TLDR
It is demonstrated that NaV1.7 knockout mice have essentially normal nociceptor activity using in vivo calcium imaging and extracellular recording, and opioid-dependent inhibition of neurotransmitter release is the principal mechanism of NaV 1.7 null analgesia in mice and humans.
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