Evidence map›Paper›PMID 36933217›Full record

ArticleCell reports2023

Somatic and terminal CB1 receptors are differentially coupled to voltage-gated sodium channels in neocortical neurons.

Luke J Steiger, Timur Tsintsadze, Glynis B Mattheisen, Stephen M Smith

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

7 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. The Retinal Light Response Is Modulated by an mGluR5-Mediated Retrograde Signal from ON-Bipolar Cells to Photoreceptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. 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

4 authors at 2 institutions in 1 country.

Luke J SteigerSection of Pulmonary and Critical Care Medicine, VA Portland Health Care System, Portland, OR, USA; Department of Medicine, Division of Pulmonary and Critical Care Medicine, Oregon Health & Science University, Portland, OR 97239, USA.
Timur TsintsadzeSection of Pulmonary and Critical Care Medicine, VA Portland Health Care System, Portland, OR, USA; Department of Medicine, Division of Pulmonary and Critical Care Medicine, Oregon Health & Science University, Portland, OR 97239, USA.
Glynis B MattheisenSection of Pulmonary and Critical Care Medicine, VA Portland Health Care System, Portland, OR, USA; Department of Medicine, Division of Pulmonary and Critical Care Medicine, Oregon Health & Science University, Portland, OR 97239, USA.
Stephen M SmithSection of Pulmonary and Critical Care Medicine, VA Portland Health Care System, Portland, OR, USA; Department of Medicine, Division of Pulmonary and Critical Care Medicine, Oregon Health & Science University, Portland, OR 97239, USA; Department of Chemical Physiology and Biochemistry, Oregon Health & Science University, Portland, OR 97239, USA. Electronic address: smisteph@ohsu.edu.
VA Portland Health Care System · USOregon Health & Science University · US

Funding

Multidisciplinary Research Training in Pulmonary MedicineT32HL083808 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI LEWINSOHN, DAVID M., SLATORE, CHRISTOPHER G. · 2008 to 2025
$5.3M
Sodium channel control of neuronal excitabilityR01GM134110 · NIGMS · OREGON HEALTH & SCIENCE UNIVERSITY · PI SMITH, STEPHEN M · 2020 to 2022
$652k
Voltage-Gated Sodium Channel Function in Neuronal Soma and TerminalsF31NS095463 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI MATTHEISEN, GLYNIS BROWN · 2015 to 2018
$117k
Dynamic Chemical Regulation of Voltage-gated Sodium ChannelsI01BX002547 · VA · PORTLAND VA MEDICAL CENTER · PI Stephen M Smith · 2015 to 2026
–
BLRD VA I01 BX002547NHLBI NIH HHS T32 HL083808NIGMS NIH HHS R01 GM134110NINDS NIH HHS F31 NS095463
6 · The paper itself

Abstract

Endogenous cannabinoid signaling is vital for important brain functions, and the same pathways can be modified pharmacologically to treat pain, epilepsy, and posttraumatic stress disorder. Endocannabinoid-mediated changes to excitability are predominantly attributed to 2-arachidonoylglycerol (2-AG) acting presynaptically via the canonical cannabinoid receptor, CB1. Here, we identify a mechanism in the neocortex by which anandamide (AEA), another major endocannabinoid, but not 2-AG, powerfully inhibits somatically recorded voltage-gated sodium channel (VGSC) currents in the majority of neurons. This pathway involves intracellular CB1 that, when activated by anandamide, decreases the likelihood of recurrent action potential generation. WIN 55,212-2 similarly activates CB1 and inhibits VGSC currents, indicating that this pathway is also positioned to mediate the actions of exogenous cannabinoids on neuronal excitability. The coupling between CB1 and VGSCs is absent at nerve terminals, and 2-AG does not block somatic VGSC currents, indicating functional compartmentalization of the actions of two endocannabinoids.

Indexed as

NeocortexVoltage-Gated Sodium ChannelsArachidonic AcidsEndocannabinoidsNeuronsPolyunsaturated AlkamidesReceptor, Cannabinoid, CB1anandamideArachidonic AcidsEndocannabinoidsPolyunsaturated AlkamidesReceptor, Cannabinoid, CB1Voltage-Gated Sodium Channelsanandamidebouton recordingcannabinoidCB1CP: Neuroscienceendocannabinoidnerve terminalsodium conductancevoltage-gated sodium channel

Identifiers

PMID36933217
PMCPMC10106091
OpenAlexW4327703917

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.