Evidence map›Paper›PMID 11606331›Full record

ArticleBritish journal of pharmacology2001

GABA receptors modulate trigeminovascular nociceptive neurotransmission in the trigeminocervical complex.

R J Storer, S Akerman, P J Goadsby

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in British journal of pharmacology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

16 citing papers in PubMed, 42 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Selective loss and transcriptional reprogramming of Nox4The journal of headache and pain · 2025
    Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Prophylactic migraine therapy: emerging treatment options.Current pain and headache reports · 2004
    Review
  15. Convergence of cervical and trigeminal sensory afferents.Current pain and headache reports · 2003
    Review
  16. Antiepileptic Drug Therapy in Migraine Headache.Current treatment options in neurology · 2002
    Article
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

3 authors at 2 institutions in 1 country.

R J StorerHeadache Group, Institute of Neurology, The National Hospital for Neurology and Neurosurgery, Queen Square, London.
S Akerman
P J Goadsby
National Hospital for Neurology and Neurosurgery · GBUniversity College London · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

1. GABA (gamma-aminobutyric acid) receptors involved in craniovascular nociceptive pathways were characterised by in vivo microiontophoresis of GABA receptor agonists and antagonists onto neurones in the trigeminocervical complex of the cat. 2. Extracellular recordings were made from neurones in the trigeminocervical complex activated by supramaximal electrical stimulation of superior sagittal sinus, which were subsequently stimulated with L-glutamate. 3. Cell firing evoked by microiontophoretic application of L-glutamate (n=30) was reversibly inhibited by GABA in every cell tested (n=19), the GABA(A) agonist muscimol (n=10) in all cells tested, or both where tested, but not by iontophoresis of either sodium or chloride ions at comparable ejection currents. Inhibited cells received wide dynamic range (WDR) or nociceptive specific input from cutaneous receptive fields on the face or forepaws. 4. The inhibition of trigeminal neurones by GABA or muscimol could be antagonized by the GABA(A) antagonist N-methylbicuculline, 1(S),9(R) in all but two cells tested (n=16), but not by the GABA(B) antagonist 2-hydroxysaclofen (n=11). 5. R(-)-baclofen, a GABA(B) agonist, inhibited the firing of three out of seven cells activated by L-glutamate. Where tested, this inhibition could be antagonized by 2-hydroxysaclofen. These baclofen-inhibited cells were characterized as having low threshold mechanoreceptor/WDR input. 6. GABA thus appears to modulate nociceptive input to the trigeminocervical complex mainly through GABA(A) receptors. GABA(A) receptors may therefore provide a target for the development of new therapeutic agents for primary headache disorders.

Indexed as

AnimalsBaclofenBicucullineCatsEvoked PotentialsGABA AgonistsGABA Antagonistsgamma-Aminobutyric AcidGlutamic AcidMuscimolNeuronsNociceptorsReceptors, GABAReceptors, GABA-AReceptors, GABA-BSynaptic Transmission2-hydroxysaclofenBaclofenBicucullinebicuculline methochlorideGABA AgonistsGABA Antagonistsgamma-Aminobutyric AcidGlutamic AcidMuscimolReceptors, GABAReceptors, GABA-AReceptors, GABA-B

Identifiers

PMID11606331
PMCPMC1573015
OpenAlexW1987819639

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.