Evidence map›Paper›PMID 12849749›Full record

ArticleNeuroscience2003

The neuronal distribution of cannabinoid receptor type 1 in the trigeminal ganglion of the rat.

T J Price, G Helesic, D Parghi, K M Hargreaves, C M Flores

Open access · greenAbstract read
In one paragraph

Article in Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
7.4field-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

76 citing papers in PubMed, 140 citations in OpenAlex.

  1. Article
  2. Article
  3. Overlapping pathways of migraine and the endocannabinoid system: Potential therapeutic targets.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Expression of Cannabinoid Receptors in the Trigeminal Ganglion of the Horse.International journal of molecular sciences · 2023
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

16 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

5 authors at 1 institution in 1 country.

T J PriceDepartment of Pharmacology, The University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.
G Helesic
D Parghi
K M Hargreaves
C M Flores
The University of Texas Health Science Center at San Antonio · US

Funding

PERIPHERAL MECHANISMS OF CANNABINOID ANTINOCICEPTIONF31DA006085 · NIDA · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI PRICE, THEODORE J · 2000 to 2002
$64k
NIDA NIH HHS F31 DA006085
6 · The paper itself

Abstract

Cannabinoid compounds have been shown to produce antinociception and antihyperalgesia by acting upon cannabinoid receptors located in both the CNS and the periphery. A potential mechanism by which cannabinoids could inhibit nociception in the periphery is the activation of cannabinoid receptors located on one or more classes of primary nociceptive neurons. To address this hypothesis, we evaluated the neuronal distribution of cannabinoid receptor type 1 (CB1) in the trigeminal ganglion (TG) of the adult rat through combined in situ hybridization (ISH) and immunohistochemistry (IHC). CB1 receptor mRNA was localized mainly to medium and large diameter neurons of the maxillary and mandibular branches of the TG. Consistent with this distribution, in a de facto nociceptive sensory neuron population that exhibited vanilloid receptor type 1 immunoreactivity, colocalization with CB1 mRNA was also sparse (<5%). Furthermore, very few neurons (approximately 5%) in the peptidergic (defined as calcitonin gene-related peptide- or substance P-immunoreactive) or the isolectin B4-binding sensory neuron populations contained CB1 mRNA. In contrast, and consistent with the neuron-size distribution for CB1, nearly 75% of CB1-positive neurons exhibited N52-immunoreactivity, a marker of myelinated axons. These results indicate that in the rat TG, CB1 receptors are expressed predominantly in neurons that are not thought to subserve nociceptive neurotransmission in the noninjured animal. Taken together with the absence of an above background in situ signal for CB2 mRNA in TG neurons, these findings suggest that the peripherally mediated antinociceptive effects of cannabinoids may involve either as yet unidentified receptors or interaction with afferent neuron populations that normally subserve non-nociceptive functions.

Indexed as

Receptor, Cannabinoid, CB2AnimalsCannabinoidsMaleNeuronsRatsRats, Sprague-DawleyReceptors, CannabinoidReceptors, DrugRNA, MessengerTrigeminal GanglionCannabinoidsCnr2 protein, ratReceptor, Cannabinoid, CB2Receptors, CannabinoidReceptors, DrugRNA, Messenger

Identifiers

PMID12849749
PMCPMC1899155
OpenAlexW2038288674

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.