Cited by 128Pancreatic function and diabetesNeuroscience and Neuropharmacology ResearchDiabetes Treatment and Management

The Influence of γ-Aminobutyric Acid on Hormone Release by the Mouse and Rat Endocrine Pancreas*

GILON, P., BERTRAND, G., LOUBATIÉRES-MARIANI, M. M., REMACLE, C., HENQUIN, J. C.·1991·Endocrinology

Abstract

The present study was aimed at localizing gamma-aminobutyric acid (GABA) and its enzyme of synthesis, glutamic acid decarboxylase (GAD), in the mouse pancreas by immunocytochemical methods. The influence of GABA on hormone release was also studied with normal mouse and rat islets and the isolated perfused rat pancreas. Particular attention was paid to glucagon release to test a recent hypothesis suggesting that GABA mediates the still unexplained glucose-induced inhibition of glucagon release. GABA and GAD were identified only in islet cells and never in the exocrine tissue. Exogenous GABA, baclofen (agonist of GABAB receptors), muscimol (agonist of GABAA receptors), or bicuculline (antagonist of GABAA receptors) did not affect insulin and somatostatin release by isolated mouse or rat islets. GABA was also without effect on glucose-induced electrical activity in mouse B-cells. Glucagon secretion by mouse islets was only slightly inhibited (approximately 20%) by GABA. Since muscimol had a similar effect, and baclofen was ineffective, the inhibition by GABA probably involves GABAA receptor activation. Bicuculline, however, did not antagonize the inhibitory effects of GABA and muscimol, probably because the antagonist alone also decreased glucagon secretion. In contrast to GABA, low (3 mM) and high (20 mM) concentrations of glucose strongly inhibited (approximately 50-65%) glucagon release; this inhibition was not prevented by bicuculline. Similar results were obtained with the…

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Crossref · 10.1210/endo-129-5-2521

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  • Expression of GABAA receptor α-subunits in mouse β-cells is very low and application of GABA does not affect GIIS.

    “Expression of GABAA receptor α-subunits in mouse β-cells is very low (Appendix Figure 13B) and application of GABA does not affect GIIS (206).”

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Authors
GILON, P., BERTRAND, G., LOUBATIÉRES-MARIANI, M. M., REMACLE, C., & HENQUIN, J. C.
Affiliations
Centre National de la Recherche Scientifique (FR)
Venue
Endocrinology
Published
1991-11
Volume
129
Issue
5
Pages
2521-2529
ISSN
  • 0013-7227 (ISSN-L)
  • 1945-7170
OpenAlex
W2096595413
Cited by
128
References
0
Citations by year
2026: 1 · 2025: 3 · 2024: 3 · 2023: 2 · 2022: 5 · 2021: 4 · 2020: 2 · 2019: 11 · 2018: 3 · 2017: 5 · 2015: 2 · 2014: 3 · 2013: 9 · 2012: 5
FWCI
2.02
Type
journal article
Language
en
Open access
closed
Locations
  • Endocrinology (publishedVersion)
  • PubMed (publishedVersion)
  • Digital Access to Libraries (Université catholique de Louvain (UCL), l'Université de Namur (UNamur) and the Université Saint-Louis (USL-B)) (submittedVersion)
Topics
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
Keywords
GABA, glutamic acid decarboxylase, glucagon secretion, GABAA receptor, GABAB receptors, pancreatic islets, alpha cells, pancreatic beta cells, insulin secretion, somatostatin secretion, bicuculline, muscimol, baclofen
MeSH terms
Animals, Female, gamma-Aminobutyric Acid, Glucagon, Glutamate Decarboxylase, Insulin, Islets of Langerhans, Membrane Potentials, Mice, Inbred Strains, Pancreatic Hormones, Rats, Inbred Strains, Somatostatin, Mice, Rats

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