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Review
. 2004 Mar;123(3):185-90.
doi: 10.1085/jgp.200409016. Epub 2004 Feb 9.

GABA in the endocrine pancreas: its putative role as an islet cell paracrine-signalling molecule

Isobel K Franklin  1 , Claes B Wollheim
Affiliations
Review

GABA in the endocrine pancreas: its putative role as an islet cell paracrine-signalling molecule

Isobel K Franklin et al. J Gen Physiol. 2004 Mar.
No abstract available

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Figures

F<sc>igure</sc> 1.
Figure 1.
Schematic diagram illustrating regulated GABA release from islet β-cell SLMVs, and the putative pathways by which it inhibits LDCV secretion in α- and β-cells. Calcium influx through voltage-dependent calcium channels (VDCC) stimulates GABA release. Secreted GABA interacts with metabotropic receptors (GABAB) and ionotropic receptors (GABAA) on recipient β- and α-cells, respectively. Receptor activation inhibits calcium entry through VDCCs, in the case of GABAA by hyperpolarizing the plasma membrane. Reduced calcium influx attenuates LDCV release in both cell types. The depicted α-cell could also represent a δ-cell, in which case somatostatin would be secreted from LDCVs in place of glucagon and glutamate. Insulin, zinc, and other products released from β-cell LDCVs probably also act as paracrine inhibitors of α-cell glucagon release.
See this image and copyright information in PMC

References

    1. Anhert-Hilger, G., A. Stadtbaumer, C. Strubing, H. Scherubl, G. Schultz, E.-O. Riecken, and B. Wiedenmann. 1996. γ-Aminobutyric acid secretion from pancreatic neuroendocrine cells. Gastroenterology. 110:1595–1604. - PubMed
    1. Braun, M., A. Wendt, B. Birnir, J. Borman, L. Eliasson, J. Galvanovskis, J. Gromada, H. Mulder, and P. Rorsman. 2004. Regulated exocytosis of GABA-containing synaptic-like microvesicles in pancreatic β cells. J. Gen. Physiol. 123:191–204. - PMC - PubMed
    1. Brice, N.L., A. Varadi, S.J.H. Ashcroft, and E. Molnar. 2002. Metabotropic glutamate and GABAB receptors contribute to the modulation of glucose-stimulated insulin secretion in pancreatic β cells. Diabetologia. 45:242–252. - PubMed
    1. Cherubini, E., J.L. Gaiarsa, and Y. Ben-Ari. 1991. GABA: an excitatory transmitter in early postnatal life. Trends Neurosci. 14:515–519. - PubMed
    1. Chessler, S.D., W.T. Simonson, I.R. Sweet, and L.P. Hammerle. 2002. Expression of the vesicular inhibitory amino acid transporter in pancreatic islet cells. Diabetes. 51:1763–1771. - PubMed

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