Evidence map›Paper›PMID 30637442›Full record

ArticleDiabetologia2019

Expression of GLP-1 receptors in insulin-containing interneurons of rat cerebral cortex.

Éva A Csajbók, Ágnes K Kocsis, Nóra Faragó, Szabina Furdan, Balázs Kovács, Sándor Lovas, Gábor Molnár, István Likó, Ágnes Zvara, László G Puskás and 2 more

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In one paragraph

Article in Diabetologia, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 16 citations in OpenAlex.

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  7. Ndnf Interneuron Excitability Is Spared in a Mouse Model of Dravet Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
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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

12 authors at 4 institutions in 1 country.

Éva A CsajbókMTA-SZTE Research Group for Cortical Microcircuits of the Hungarian Academy of Sciences, Department of Physiology, Anatomy and Neuroscience, University of Szeged, Közép fasor 52, Szeged, H-6726, Hungary.
Ágnes K KocsisMTA-SZTE Research Group for Cortical Microcircuits of the Hungarian Academy of Sciences, Department of Physiology, Anatomy and Neuroscience, University of Szeged, Közép fasor 52, Szeged, H-6726, Hungary.
Nóra FaragóMTA-SZTE Research Group for Cortical Microcircuits of the Hungarian Academy of Sciences, Department of Physiology, Anatomy and Neuroscience, University of Szeged, Közép fasor 52, Szeged, H-6726, Hungary.
Szabina FurdanMTA-SZTE Research Group for Cortical Microcircuits of the Hungarian Academy of Sciences, Department of Physiology, Anatomy and Neuroscience, University of Szeged, Közép fasor 52, Szeged, H-6726, Hungary.
Balázs KovácsMTA-SZTE Research Group for Cortical Microcircuits of the Hungarian Academy of Sciences, Department of Physiology, Anatomy and Neuroscience, University of Szeged, Közép fasor 52, Szeged, H-6726, Hungary.
Sándor LovasMTA-SZTE Research Group for Cortical Microcircuits of the Hungarian Academy of Sciences, Department of Physiology, Anatomy and Neuroscience, University of Szeged, Közép fasor 52, Szeged, H-6726, Hungary.
Gábor MolnárMTA-SZTE Research Group for Cortical Microcircuits of the Hungarian Academy of Sciences, Department of Physiology, Anatomy and Neuroscience, University of Szeged, Közép fasor 52, Szeged, H-6726, Hungary.
István LikóMTA Lendület Hereditary Endocrine Tumors Research Group, Semmelweis University, Budapest, Hungary.
Ágnes ZvaraLaboratory of Functional Genomics, Institute of Genetics, Biological Research Center, Hungarian Academy of Sciences, Szeged, Hungary.
László G PuskásLaboratory of Functional Genomics, Institute of Genetics, Biological Research Center, Hungarian Academy of Sciences, Szeged, Hungary.
Attila PatócsMTA Lendület Hereditary Endocrine Tumors Research Group, Semmelweis University, Budapest, Hungary.
Gábor TamásMTA-SZTE Research Group for Cortical Microcircuits of the Hungarian Academy of Sciences, Department of Physiology, Anatomy and Neuroscience, University of Szeged, Közép fasor 52, Szeged, H-6726, Hungary. gtamas@bio.u-szeged.hu.
Hungarian Academy of Sciences · HUUniversity of Szeged · HUSemmelweis University · HUInstitute of Genetics · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisGlucagon-like peptide 1 (GLP-1) receptors are expressed by pancreatic beta cells and GLP-1 receptor signalling promotes insulin secretion. GLP-1 receptor agonists have neural effects and are therapeutically promising for mild cognitive impairment and Alzheimer's disease. Our previous results showed that insulin is released by neurogliaform neurons in the cerebral cortex, but the expression of GLP-1 receptors on insulin-producing neocortical neurons has not been tested. In this study, we aimed to determine whether GLP-1 receptors are present in insulin-containing neurons.

methodsWe harvested the cytoplasm of electrophysiologically and anatomically identified neurogliaform interneurons during patch-clamp recordings performed in slices of rat neocortex. Using single-cell digital PCR, we determined copy numbers of Glp1r mRNA and other key genes in neurogliaform cells harvested in conditions corresponding to hypoglycaemia (0.5 mmol/l glucose) and hyperglycaemia (10 mmol/l glucose). In addition, we performed whole-cell patch-clamp recordings on neurogliaform cells to test the effects of GLP-1 receptor agonists for functional validation of single-cell digital PCR results.

resultsSingle-cell digital PCR revealed GLP-1 receptor expression in neurogliaform cells and showed that copy numbers of mRNA of the Glp1r gene in hyperglycaemia exceeded those in hypoglycaemia by 9.6 times (p < 0.008). Moreover, single-cell digital PCR confirmed co-expression of Glp1r and Ins2 mRNA in neurogliaform cells. Functional expression of GLP-1 receptors was confirmed with whole-cell patch-clamp electrophysiology, showing a reversible effect of GLP-1 on neurogliaform cells. This effect was prevented by pre-treatment with the GLP-1 receptor-specific antagonist exendin-3(9-39) and was absent in hypoglycaemia. In addition, single-cell digital PCR of neurogliaform cells revealed that the expression of transcription factors (Pdx1, Isl1, Mafb) are important in beta cell development. CONCLUSIONS/

interpretationOur results provide evidence for the functional expression of GLP-1 receptors in neurons known to release insulin in the cerebral cortex. Hyperglycaemia increases the expression of GLP-1 receptors in neurogliaform cells, suggesting that endogenous incretins and therapeutic GLP-1 receptor agonists might have effects on these neurons, similar to those in pancreatic beta cells.

Indexed as

AnimalsCerebral CortexCytoplasmGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorHyperglycemiaHypoglycemiaInsulinInterneuronsMaleNeocortexRatsRats, WistarSignal TransductionGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorInsulinAnimalBasic scienceGastro-entero pancreatic factorsHormone receptorsOther techniquesRat

Identifiers

PMID30637442
OpenAlexW2910746539

What Socratic holds

Textmetadata
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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 Socratic graph.