Authors
Austin E Stis, Charles S Lazimi, Sandra M Ferreira, Alexandra E Cuaycal, Dylan Smurlick, D Walker Hagan, Taylor Nakayama, Sunil P Gandhi, Emery Smith, Timothy P Spicer, Edward A Phelps
Published in
Molecular metabolism. Pages 102447. Sep 25, 2026. Epub Sep 25, 2026.
Abstract
Pancreatic beta cells have the unique function of synthesizing and secreting high amounts of the inhibitory neurotransmitter γ-aminobutyric acid (GABA). The mechanism of GABA secretion, whether vesicular or channel-mediated, is debated. Our study reveals surprising temporal complexity in the pattern of islet GABA secretion. We used insulin secretion modulators to demonstrate that GABA release is not directly correlated with insulin secretion. VGAT reporter mice also showed that beta cells do not express the requisite vesicular GABA transporter (VGAT) for vesicular GABA release. Instead, GABA is secreted from the cytosol in pulses that depend on expression of the LRRC8D subunit of the volume regulatory anion channel (VRAC). We further demonstrate the dynamic coordination of GABA release with calcium influx in beta cells and dependence on beta cell depolarization. These results suggest a model where GABA is released during the peaks of beta cell calcium oscillations to provide feedback which strengthens and reinforces the oscillation waveform.
PMID:
42790701
Bibliographic data and abstract were imported from PubMed on 26 Sep 2026.
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