Evidence map›Paper›PMID 23112192›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Critical role of calcitonin gene-related peptide receptors in cortical spreading depression.

Alessandro Tozzi, Antonio de Iure, Massimiliano Di Filippo, Cinzia Costa, Stefano Caproni, Antonio Pisani, Paola Bonsi, Barbara Picconi, Letizia M Cupini, Serena Materazzi and 3 more

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In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

79 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Systematic review of the pharmacological agents that have been tested against spreading depolarizations.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018
    Pooled it
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19 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

13 authors.

Alessandro TozziClinica Neurologica, Università di Perugia, 06156 Perugia, Italy.
Antonio de Iure
Massimiliano Di Filippo
Cinzia Costa
Stefano Caproni
Antonio Pisani
Paola Bonsi
Barbara Picconi
Letizia M Cupini
Serena Materazzi
Pierangelo Geppetti
Paola Sarchielli
Paolo Calabresi

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cortical spreading depression (CSD) is a key pathogenetic step in migraine with aura. Dysfunctions of voltage-dependent and receptor-operated channels have been implicated in the generation of CSD and in the pathophysiology of migraine. Although a known correlation exists between migraine and release of the calcitonin gene-related peptide (CGRP), the possibility that CGRP is involved in CSD has not been examined in detail. We analyzed the pharmacological mechanisms underlying CSD and investigated the possibility that endogenous CGRP contributes to this phenomenon. CSD was analyzed in rat neocortical slices by imaging of the intrinsic optical signal. CSD was measured as the percentage of the maximal surface of a cortical slice covered by the propagation of intrinsic optical signal changes during an induction episode. Reproducible CSD episodes were induced through repetitive elevations of extracellular potassium concentration. AMPA glutamate receptor antagonism did not inhibit CSD, whereas NMDA receptor antagonism did inhibit CSD. Blockade of voltage-dependent sodium channels by TTX also reduced CSD. CSD was also decreased by the antiepileptic drug topiramate, but not by carbamazepine. Interestingly, endogenous CGRP was released in the cortical tissue in a calcium-dependent manner during CSD, and three different CGRP receptor antagonists had a dose-dependent inhibitory effect on CSD, suggesting a critical role of CGRP in this phenomenon. Our findings show that both glutamate NMDA receptors and voltage-dependent sodium channels play roles in CSD. They also demonstrate that CGRP antagonism reduces CSD, supporting the possible use of drugs targeting central CGRP receptors as antimigraine agents.

Indexed as

AnimalsAnticonvulsantsCalcitonin Gene-Related PeptideCalcitonin Gene-Related Peptide Receptor AntagonistsCarbamazepineCerebral CortexCortical Spreading DepressionDose-Response Relationship, DrugFructoseMaleMigraine DisordersRatsRats, WistarReceptors, AMPAReceptors, Calcitonin Gene-Related PeptideReceptors, N-Methyl-D-AspartateAnticonvulsantsCalcitonin Gene-Related PeptideCalcitonin Gene-Related Peptide Receptor AntagonistsCarbamazepineFructoseReceptors, AMPAReceptors, Calcitonin Gene-Related PeptideReceptors, N-Methyl-D-AspartateTopiramateVoltage-Gated Sodium Channels

Identifiers

PMID23112192
PMCPMC3503217

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.