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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
Free PMC article
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.
Free PMC article
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.
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