Evidence map›Paper›PMID 33180836›Full record

ArticlePloS one2020

Lactate induces synapse-specific potentiation on CA3 pyramidal cells of rat hippocampus.

Gabriel Herrera-López, Ernesto Griego, Emilio J Galván

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 37 citations in OpenAlex.

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  20. Activation of lactate receptor HCAR1 down-modulates neuronal activity in rodent and human brain tissue.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022
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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 1 institution in 1 country.

Gabriel Herrera-LópezDepartamento de Farmacobiología, Cinvestav Sede Sur, México City, México.
Ernesto GriegoDepartamento de Farmacobiología, Cinvestav Sede Sur, México City, México.ORCID 0000-0003-2396-9271
Emilio J GalvánDepartamento de Farmacobiología, Cinvestav Sede Sur, México City, México.ORCID 0000-0002-9820-302X
Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuronal activity within the physiologic range stimulates lactate production that, via metabolic pathways or operating through an array of G-protein-coupled receptors, regulates intrinsic excitability and synaptic transmission. The recent discovery that lactate exerts a tight control of ion channels, neurotransmitter release, and synaptic plasticity-related intracellular signaling cascades opens up the possibility that lactate regulates synaptic potentiation at central synapses. Here, we demonstrate that extracellular lactate (1-2 mM) induces glutamatergic potentiation on the recurrent collateral synapses of hippocampal CA3 pyramidal cells. This potentiation is independent of lactate transport and further metabolism, but requires activation of NMDA receptors, postsynaptic calcium accumulation, and activation of a G-protein-coupled receptor sensitive to cholera toxin. Furthermore, perfusion of 3,5- dihydroxybenzoic acid, a lactate receptor agonist, mimics this form of synaptic potentiation. The transduction mechanism underlying this novel form of synaptic plasticity requires G-protein βγ subunits, inositol-1,4,5-trisphosphate 3-kinase, PKC, and CaMKII. Activation of these signaling cascades is compartmentalized in a synapse-specific manner since lactate does not induce potentiation at the mossy fiber synapses of CA3 pyramidal cells. Consistent with this synapse-specific potentiation, lactate increases the output discharge of CA3 neurons when recurrent collaterals are repeatedly activated during lactate perfusion. This study provides new insights into the cellular mechanisms by which lactate, acting via a membrane receptor, contributes to the memory formation process.

Indexed as

AnimalsCA3 Region, HippocampalCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Cholera ToxinExcitatory Postsynaptic PotentialsLactic AcidMaleNeuronal PlasticityOxamic AcidProtein Kinase CRatsRats, Sprague-DawleyReceptors, N-Methyl-D-AspartateSignal TransductionSynapsesCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Cholera ToxinLactic AcidOxamic AcidProtein Kinase CReceptors, N-Methyl-D-Aspartate

Identifiers

PMID33180836
PMCPMC7660554
OpenAlexW3100952479

What OpenQuestion holds

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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.