Evidence map›Paper›PMID 40736941›Full record

ArticleMolecular neurobiology2025

Single Electrically Induced Epileptic Afterdischarge Triggers Synaptic Weakening, AMPA Receptor Endocytosis, and Shrinkage of Dendritic Spines in the Hippocampus.

Ana Paula Crestani, Leonardo Rakauskas Zacharias, Danilo Benette Marques, Flavia Faria Formagio Fonseca, Rafael Naime Ruggiero, João Pereira Leite

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Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

1 citing paper in PubMed.

  1. 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

6 authors.

Ana Paula CrestaniDepartment of Neuroscience and Behavioral Sciences, Ribeirão Preto Medical Schools, University of São Paulo, Ribeirão Preto, SP, Brazil. paula.crestani@gmail.com.ORCID http://orcid.org/0000-0003-0867-9524
Leonardo Rakauskas Zacharias *Department of Neuroscience and Behavioral Sciences, Ribeirão Preto Medical Schools, University of São Paulo, Ribeirão Preto, SP, Brazil.ORCID http://orcid.org/0000-0002-5973-8654
Danilo Benette Marques *Department of Neuroscience and Behavioral Sciences, Ribeirão Preto Medical Schools, University of São Paulo, Ribeirão Preto, SP, Brazil.ORCID http://orcid.org/0000-0002-8293-8822
Flavia Faria Formagio FonsecaDepartment of Neuroscience and Behavioral Sciences, Ribeirão Preto Medical Schools, University of São Paulo, Ribeirão Preto, SP, Brazil.
Rafael Naime RuggieroDepartment of Neuroscience and Behavioral Sciences, Ribeirão Preto Medical Schools, University of São Paulo, Ribeirão Preto, SP, Brazil.ORCID http://orcid.org/0000-0002-4712-6853
João Pereira LeiteDepartment of Neuroscience and Behavioral Sciences, Ribeirão Preto Medical Schools, University of São Paulo, Ribeirão Preto, SP, Brazil.ORCID http://orcid.org/0000-0003-0558-3519

Funding

São Paulo Research Foundation (FAPESP), Brazil 2016/17882-4São Paulo Research Foundation (FAPESP), Brazil 2018/02303-4São Paulo Research Foundation (FAPESP), Brazil 2018/18014-1São Paulo Research Foundation (FAPESP), Brazil 2024/15007-5
6 · The paper itself

Abstract

Afterdischarge (AD) is an experimental model of electrically induced seizures. When induced in limbic structures, AD is known to induce acute behavioral alterations and flattening of local field potentials that persist for a few minutes. However, impairments in more complex cognitive processes such as learning and memory can last for hours after the seizure. Considering the mismatch between ephemeral postictal electrophysiological changes and long-lasting cognitive impairments, synaptic plasticity emerges as a possible mechanism that integrates these findings. Therefore, we used a multilevel approach to evaluate the effects of a single AD on synaptic plasticity in rats. First, we showed that a single AD-eliciting stimulation at the perforant pathway-dentate gyrus (PP-DG) synapse causes long-lasting decrease of evoked postsynaptic potentials. Then, we observed that this functional alteration was accompanied by shrinkage of mushroom-shaped spines in the DG. Lastly, reduced levels of p(Ser845)-GluA1 and GluA1 subunits of AMPA receptors (AMPARs) were found in the hippocampal postsynaptic density. Together, our data suggest that an AD induces a long-term depression (LTD)-like synaptic plasticity phenomenon, which is characterized by synaptic weakening, AMPAR endocytosis, and dendritic spine shrinkage. Furthermore, the postictal changes in synaptic plasticity observed here align with the course of cognitive impairments often reported in other studies.

Indexed as

Dendritic SpinesEndocytosisEpilepsyHippocampusReceptors, AMPASynapsesAnimalsElectric StimulationLong-Term Synaptic DepressionMaleNeuronal PlasticityRatsRats, WistarReceptors, AMPAAfterdischargeAMPARDendritic spinesHippocampusSynaptic weakening

Identifiers

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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 Socratic graph.