Evidence map›Paper›PMID 25740514›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015

Cannabinoid CB1 receptor calibrates excitatory synaptic balance in the mouse hippocampus.

Krisztina Monory, Martin Polack, Anita Remus, Beat Lutz, Martin Korte

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
9.6field-weighted citation impact, top 2% 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

41 citing papers in PubMed, 107 citations in OpenAlex.

  1. The endocannabinoid system and the ageing brain.Nature reviews. Neuroscience · 2026
    Review
  2. Review
  3. Review
  4. Genetic Tools in Rodents to Study Cannabinoid Functions.Current topics in behavioral neurosciences · 2026
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. CB1R activates the epilepsy-associated protein Go to regulate neurotransmitter release and synaptic plasticity in the cerebellum.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. APPsα Rescues Tau-Induced Synaptic Pathology.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  17. Review
  18. 2-AG and anandamide enhance hippocampal long-term potentiationFrontiers in cellular neuroscience · 2022
    Article
  19. Article
  20. 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

5 authors at 2 institutions in 2 countries.

Krisztina MonoryInstitute of Physiological Chemistry, Medical Center of the Johannes Gutenberg University Mainz, 55128 Mainz, Germany.
Martin PolackZoological Institute, Division Cellular Neurobiology, 38106 Braunschweig, Germany, and.
Anita RemusZoological Institute, Division Cellular Neurobiology, 38106 Braunschweig, Germany, and AG NIND, HZI, D-38124 Braunschweig, Germany.
Beat LutzInstitute of Physiological Chemistry, Medical Center of the Johannes Gutenberg University Mainz, 55128 Mainz, Germany.
Martin KorteZoological Institute, Division Cellular Neurobiology, 38106 Braunschweig, Germany, and AG NIND, HZI, D-38124 Braunschweig, Germany m.korte@tu-bs.de.
University Medical Center of the Johannes Gutenberg University Mainz · DEZoological Institute · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The endocannabinoid system negatively regulates the release of various neurotransmitters in an activity-dependent manner, thereby influencing the excitability of neuronal circuits. In the hippocampus, cannabinoid type 1 (CB1) receptor is present on both GABAergic and glutamatergic axon terminals. CB1 receptor-deficient mice were previously shown to have increased hippocampal long-term potentiation (LTP). In this study, we have investigated the consequences of cell-type-specific deletion of the CB1 receptor on the induction of hippocampal LTP and on CA1 pyramidal cell morphology. Deletion of CB1 receptor in GABAergic neurons in GABA-CB1-KO mice leads to a significantly decreased hippocampal LTP compared with WT controls. Concomitantly, CA1 pyramidal neurons have a significantly reduced dendritic branching both on the apical and on the basal dendrites. Moreover, the average spine density on the apical dendrites of CA1 pyramidal neurons is significantly diminished. In contrast, in mice lacking CB1 receptor in glutamatergic cells (Glu-CB1-KO), hippocampal LTP is significantly enhanced and CA1 pyramidal neurons show an increased branching and an increased spine density in the apical dendritic region. Together, these results indicate that the CB1 receptor signaling system both on inhibitory and excitatory neurons controls functional and structural synaptic plasticity of pyramidal neurons in the hippocampal CA1 region to maintain an appropriate homeostatic state upon neuronal activation. Consequently, if the CB1 receptor is lost in either neuronal population, an allostatic shift will occur leading to a long-term dysregulation of neuronal functions.

Indexed as

AnimalsExcitatory Postsynaptic PotentialsHippocampusLong-Term PotentiationMiceMice, Inbred C57BLMice, KnockoutNeuronal PlasticityReceptor, Cannabinoid, CB1SynapsesSynaptic TransmissionReceptor, Cannabinoid, CB1cannabinoidsCB1 receptordendritic morphologyLTPspinessynaptic plasticity

Identifiers

PMID25740514
PMCPMC6605579
OpenAlexW1973431395

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.