Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Ion channel activities implicated in pathological pain.

John N Wood1, Bjarke Abrahamsen, Mark D Baker

  • 1Molecular Nociception Group, andLondon Pain Consortium, Department of Biology, University College London, Gover Street, London WC1E 6BT, UK.

Novartis Foundation Symposium
|October 8, 2004
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Fasciclin 2 engages EGFR in an auto-stimulatory loop to promote imaginal disc cell proliferation in Drosophila.

PLoS genetics·2022
Same author

Mapping of Danish Pharmacy Technician Students' Third-Year Projects in a Year with the COVID-19 Pandemic.

Pharmacy (Basel, Switzerland)·2022
Same author

For which patient subgroups are there positive outcomes from a medication review? A systematic review.

Pharmacy practice·2020
Same author

Using Real-Life Data to Strengthen the Education of Pharmacy Technician Students: From Student to Research Assistant.

Pharmacy (Basel, Switzerland)·2020
Same author

Pharmaceutical care services available in Danish community pharmacies.

International journal of clinical pharmacy·2020
Same author

Customers' information seeking behavior prior to community pharmacy visits: A community pharmacy survey.

Research in social & administrative pharmacy : RSAP·2020
Same journal

Genetic and therapeutic control of diabetogenic CD8+ T cells.

Novartis Foundation symposium·2009
Same journal

Translating mucosal antigen based prevention of autoimmune diabetes to human.

Novartis Foundation symposium·2009
Same journal

Re-establishing immune tolerance in type 1 diabetes via regulatory T cells.

Novartis Foundation symposium·2009
Same journal

Immune markers of disease and therapeutic intervention in type 1 diabetes.

Novartis Foundation symposium·2009
Same journal

Towards a curative therapy in type 1 diabetes: remission of autoimmunity, maintenance and augmentation of beta cell mass.

Novartis Foundation symposium·2009
Same journal

CD8 and cytotoxic T cells in type 1 diabetes.

Novartis Foundation symposium·2009
See all related articles

Altered ion channel expression contributes to neuropathic pain. This chapter reviews evidence for post-translational regulation of Nav1.9 and discusses candidate mechanosensors like TRP channels in pain signaling.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pain Research

Background:

  • Neuropathic pain involves altered expression of voltage-gated ion channels (sodium, calcium, potassium) and ligand-gated receptors (P2X3, NMDA).
  • Pacemaker HCN channels are also implicated in neuropathic pain pathogenesis.
  • The molecular identity of mechanosensors in sensory neurons, crucial for tactile allodynia and mechanical hyperalgesia, remains largely unknown.

Purpose of the Study:

  • To present evidence for the role of post-translational regulation of Nav1.9 in pain thresholds.
  • To review candidate mechanosensor genes, including acid-sensing ion channels (ASICs) and transient receptor potential (TRP) channels.
  • To discuss the use of gene deletion approaches to understand ion channel function in sensory neuron excitability and pain.

Main Methods:

Related Experiment Videos

  • Review of existing literature on ion channel function in neuropathic pain.
  • Analysis of evidence for and against the role of ASICs in mechanotransduction.
  • Examination of recent findings implicating TRP channels in mechanosensation.
  • Discussion of sensory neuron-specific gene deletion strategies.

Main Results:

  • Evidence supports a significant role for post-translational regulation of Nav1.9 in determining pain sensitivity.
  • ASICs are unlikely to function as primary mechanotransducers in sensory neurons.
  • TRP channels are increasingly implicated in the process of mechanosensation.

Conclusions:

  • Ion channel regulation, particularly post-translational modifications of Nav1.9, is critical for pain threshold control.
  • TRP channels represent promising candidates for sensory mechanotransduction, warranting further investigation.
  • Targeted genetic approaches are essential for elucidating the specific roles of individual ion channels in pain pathways.