Evidence map›Paper›PMID 19144838›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009

Glutamatergic modulation of cerebellar interneuron activity is mediated by an enhancement of GABA release and requires protein kinase A/RIM1alpha signaling.

Philippe M Lachamp, Yu Liu, Siqiong June Liu

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

26 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Advances in the Electrophysiological Recordings of Long-Term Potentiation.International journal of molecular sciences · 2023
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Fasting induces a form of autonomic synaptic plasticity that prevents hypoglycemia.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  13. Article
  14. Article
  15. Article
  16. Presynaptic long-term plasticity.Frontiers in synaptic neuroscience · 2013
    Review
  17. Review
  18. Review
  19. Article
  20. Presynaptic LTP and LTD of excitatory and inhibitory synapses.Cold Spring Harbor perspectives in biology · 2012
    Review
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.

Philippe M LachampDepartment of Biology, Pennsylvania State University, State College, Pennsylvania 16802, USA.
Yu Liu
Siqiong June Liu
Pennsylvania State University · USThe University of Texas Southwestern Medical Center · US

Funding

Cellular Mechanisms Underlying the Long-term Potentiation of GABA ReleaseR01NS058867 · NINDS · PENNSYLVANIA STATE UNIVERSITY, THE · PI LIU, SIQIONG JUNE · 2007 to 2011
$1.4M
NINDS NIH HHS NS58867NINDS NIH HHS R01 NS058867
6 · The paper itself

Abstract

Information processing in the CNS is controlled by the activity of neuronal networks composed of principal neurons and interneurons. Activity-dependent modification of synaptic transmission onto principal neurons is well studied, but little is known about the modulation of inhibitory transmission between interneurons. However, synaptic plasticity at this level has clear implications for the generation of synchronized activity. We investigated the molecular mechanism(s) and functional consequences of an activity-induced lasting increase in GABA release that occurs between inhibitory interneurons (stellate cells) in the cerebellum. Using whole-cell recording and cerebellar slices, we found that stimulation of glutamatergic inputs (parallel fibers) with a physiological-like pattern of activity triggered a lasting increase in GABA release from stellate cells. This activity also potentiated inhibitory transmission between synaptically connected interneurons. Extracellular recording revealed that the enhanced inhibitory transmission reduced the firing frequency and altered the pattern of action potential activity in stellate cells. The induction of the sustained increase in GABA release required activation of NMDA receptors. Using pharmacological and genetic approaches, we found that presynaptic cAMP/PKA (protein kinase A) signaling and RIM1alpha, an active zone protein, is the critical pathway that is required for the lasting enhancement of GABA release. Thus, a common mechanism can underlie presynaptic plasticity of both excitatory and inhibitory transmission. This activity-dependent regulation of synaptic transmission between inhibitory interneurons may serve as an important mechanism for interneuronal network plasticity.

Indexed as

Action PotentialsAnimalsAnimals, NewbornCerebellumCyclic AMPCyclic AMP-Dependent Protein KinasesElectric StimulationEnzyme InhibitorsExcitatory Amino Acid AgonistsGABA Antagonistsgamma-Aminobutyric AcidGlutamic AcidGlycineGTP-Binding ProteinsInterneuronsIn Vitro TechniquesCyclic AMPCyclic AMP-Dependent Protein KinasesEnzyme InhibitorsExcitatory Amino Acid AgonistsGABA Antagonistsgabazinegamma-Aminobutyric AcidGlutamic AcidGlycineGTP-Binding ProteinsN-MethylaspartatePyridazinesRims1 protein, mouse

Identifiers

PMID19144838
PMCPMC2775555
OpenAlexW2063731880

What OpenQuestion holds

Textmetadata
LicenceTDM
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.