Evidence map›Paper›PMID 12451128›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002

Roles of tetrodotoxin (TTX)-sensitive Na+ current, TTX-resistant Na+ current, and Ca2+ current in the action potentials of nociceptive sensory neurons.

Nathaniel T Blair, Bruce P Bean

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 236 papers.

0numbers the graph read from it
0cells of the map it votes in
236citing papers in PubMed
5.8field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

236 citing papers in PubMed, 419 citations in OpenAlex.

  1. Channels (Austin, Tex.) · 2026
    Article
  2. Article
  3. Article
  4. Targeting Supramolecular Active Complexes of NaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  5. Article
  6. The psychoactive cannabinoid THC inhibits peripheral nociceptors by targeting NaNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Sulfolipid-1 fromJournal of neurophysiology · 2026
    Article
  11. Shaping the Action Potential in Dorsal Root and Trigeminal Ganglia Neurons: Relevance to Pain Mechanisms.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Review
  12. Article
  13. Review
  14. Nav1.8: Intrinsic limits on the functional effect of abrogation in DRG neurons.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  15. Critical role of extracellular loops in differential modulations of TTX-sensitive and TTX-resistant NaProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  16. Article
  17. Article
  18. Review
  19. Modulation of human dorsal root ganglion neuron firing by the Nav1.8 inhibitor suzetrigine.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  20. Article

176 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Nathaniel T BlairDepartment of Neurobiology, Harvard Medical School, Boston, Massachusetts 20114, USA. nathaniel_blair@student.hms.harvard.edu
Bruce P Bean
Harvard University · US

Funding

VOLTAGE DEPENDENT ION CHANNELS IN PURKINJE NEURONSR01NS036855 · NINDS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI BEAN, BRUCE P · 1997 to 2022
$7.7M
MUSCARINIC MODULATION OF GIRK CHANNELS IN THE CNSP01NS038312 · NINDS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI BEAN, BRUCE P · 1999 to 2003
$3.9M
Voltage-dependent ion channels in Purkinje neuronsR37NS036855 · NINDS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI BEAN, BRUCE P · 2002 to 2008
$2.8M
NEUROTRANSMITTER CONTROL OF IONIC CHANNELSR01HL035034 · NHLBI · OREGON HEALTH AND SCIENCE UNIVERSITY · PI BEAN, BRUCE P · 1985 to 2001
$705k
NHLBI NIH HHS HL35034NINDS NIH HHS NS36855NINDS NIH HHS NS38312NINDS NIH HHS R01 NS036855NINDS NIH HHS R37 NS036855
6 · The paper itself

Abstract

Nociceptive sensory neurons are unusual in expressing voltage-gated inward currents carried by sodium channels resistant to block by tetrodotoxin (TTX) as well as currents carried by conventional TTX-sensitive sodium channels and voltage-dependent calcium channels. To examine how currents carried by each of these helps to shape the action potential in small-diameter dorsal root ganglion cell bodies, we voltage clamped cells by using the action potential recorded from each cell as the command voltage. Using intracellular solutions of physiological ionic composition, we isolated individual components of current flowing during the action potential with the use of channel blockers (TTX for TTX-sensitive sodium currents and a mixture of calcium channel blockers for calcium currents) and ionic substitution (TTX-resistant current measured by the replacement of extracellular sodium by N-methyl-D-glucamine in the presence of TTX, with correction for altered driving force). TTX-resistant sodium channels activated quickly enough to carry the largest inward charge during the upstroke of the nociceptor action potential (approximately 58%), with TTX-sensitive sodium channels also contributing significantly ( approximately 40%), especially near threshold, and high voltage-activated calcium currents much less (approximately 2%). Action potentials had a prominent shoulder during the falling phase, characteristic of nociceptive neurons. TTX-resistant sodium channels did not inactivate completely during the action potential and carried the majority (58%) of inward current flowing during the shoulder, with high voltage-activated calcium current also contributing significantly (39%). Unlike calcium current, TTX-resistant sodium current is not accompanied by opposing calcium-activated potassium current and may provide an effective mechanism by which the duration of action potentials (and consequently calcium entry) can be regulated.

Indexed as

Action PotentialsAnimalsCalciumCapsaicinCells, CulturedElectrophysiologyGanglia, SpinalNeurons, AfferentNociceptorsPatch-Clamp TechniquesRatsRats, Long-EvansSodiumSodium Channel BlockersSodium ChannelsTetrodotoxinCalciumCapsaicinSodiumSodium Channel BlockersSodium ChannelsTetrodotoxin

Identifiers

PMID12451128
PMCPMC6758735
OpenAlexW2162723169

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.