Evidence map›Paper›PMID 36805257›Full record

ArticleNeuro-oncology2023

Molecular changes underlying decay of sensory responses and enhanced seizure propensity in peritumoral neurons.

Elena Tantillo, Marta Scalera, Elisa De Santis, Nicolò Meneghetti, Chiara Cerri, Michele Menicagli, Alberto Mazzoni, Mario Costa, Chiara Maria Mazzanti, Eleonora Vannini and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Neuro-oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 25% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.

  1. Pooled it
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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

11 authors at 5 institutions in 1 country.

Elena TantilloCNR Neuroscience Institute, Pisa, Italy.
Marta ScaleraCNR Neuroscience Institute, Pisa, Italy.
Elisa De SantisCNR Neuroscience Institute, Pisa, Italy.
Nicolò MeneghettiFondazione Pisana per la Scienza Onlus (FPS) Pisa, Italy.ORCID 0000-0002-3466-0504
Chiara CerriFondazione Umberto Veronesi, Milan, Italy.
Michele Menicagli
Alberto MazzoniThe Biorobotics Institute, Scuola Superiore Sant'Anna, Pisa, Italy.
Mario CostaCNR Neuroscience Institute, Pisa, Italy.
Chiara Maria MazzantiFondazione Pisana per la Scienza Onlus (FPS) Pisa, Italy.
Eleonora VanniniCNR Neuroscience Institute, Pisa, Italy.ORCID 0000-0002-1337-3901
Matteo CaleoCNR Neuroscience Institute, Pisa, Italy.
Fondazione Pisa · ITNeuroscience Institute · ITScuola Superiore Sant'Anna · ITUniversity of Padua · ITUniversity of Pisa · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGlioblastoma growth impacts on the structure and physiology of peritumoral neuronal networks, altering the activity of pyramidal neurons which drives further tumor progression. It is therefore of paramount importance to identify glioma-induced changes in pyramidal neurons, since they represent a key therapeutic target.

methodsWe longitudinal monitored visual evoked potentials after the orthotopic implant of murine glioma cells into the mouse occipital cortex. With laser microdissection, we analyzed layer II-III pyramidal neurons molecular profile and with local field potentials recordings we evaluated the propensity to seizures in glioma-bearing animals with respect to control mice.

resultsWe determine the time course of neuronal dysfunction of glioma-bearing mice and we identify a symptomatic stage, based on the decay of visual response. At that time point, we microdissect layer II-III pyramidal neurons and evaluate the expression of a panel of genes involved in synaptic transmission and neuronal excitability. Compared to the control group, peritumoral neurons show a decrease in the expression of the SNARE complex gene SNAP25 and the alpha1 subunit of the GABA-A receptor. No significant changes are detected in glutamatergic (ie, AMPA or NMDA receptor subunit) markers. Further reduction of GABA-A signaling by delivery of a benzodiazepine inverse agonist, DMCM (methyl-6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate) precipitates seizures in 2 mouse models of tumor-bearing mice.

conclusionsThese studies reveal novel molecular changes that occur in the principal cells of the tumor-adjacent zone. These modifications may be therapeutically targeted to ameliorate patients' quality of life.

Indexed as

Evoked Potentials, VisualGliomaAnimalsDrug Inverse AgonismMiceNeuronsQuality of LifeSeizuresgliomalaser capturemicrodissectionmouse modelseizurevisual cortex

Identifiers

PMID36805257
PMCPMC10398807
OpenAlexW4321372113

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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 OpenQuestion graph.