Abstract
Immunocytochemistry was carried out on sections of rat pancreas to localize the expression of glutamate receptor subunits and the major pancreatic peptide hormones. Glutamate receptor expression was concentrated in pancreatic islets, and each islet cell type expressed different neuronal glutamate receptors of the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) and kainate classes. AMPA receptor subunits were expressed in alpha, beta, and pancreatic polypeptide cells, whereas kainate receptors were found predominantly in alpha and delta cells. Patch clamp electrophysiology was used to measure the functional properties of islet cell glutamate receptors. L-glutamate and other glutamate receptor agonists evoked currents in islet cells that were blocked by the selective AMPA receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione and potentiated by cyclothiazide in a manner indistinguishable from that of neuronal AMPA receptors. Activation of islet cell AMPA receptors produced steady-state cation currents that depolarized the cells an average of 20.7 +/- 5.4 mV (n = 6). Currents mediated by functional kainate receptors were also observed in a line of transformed pancreatic alpha cells. Thus, L-glutamate probably regulates islet physiology via actions at both AMPA and kainate receptor classes. The pattern of receptor expression suggests that glutamate receptor activation may have multiple, complex consequences for islet physiology.
Highlights
Teins, and energy levels, but very few of them respond directly to extracellular stimuli
An antibody against insulin stained the core of the islets and was used as marker for  cells, an antibody that recognizes glucagon stained ␣ cells, ␦ cells were labeled with a somatostatin antibody, and cells positive for pancreatic polypeptide were referred to as PP cells
Using complementary approaches we have shown that pancreatic islet cells express glutamate receptors of the amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) and kainate classes
Summary
Teins, and energy levels, but very few of them respond directly to extracellular stimuli. ␥-amino butyric acid (GABA)-A receptors have been observed in many pancreatic islet cells Activation of these receptors inhibits glucagon secretion [3] and depolarizes some types of  cell lines [4]. Nitroquinoxaline-2,3-dione and potentiated by cy- Mechanisms whereby glutamate receptor activation may clothiazide in a manner indistinguishable from that of control hormone secretion from pancreas or preparations of neuronal AMPA receptors. Currents mediated by functional kainate receptors were observed in a line of transformed pancreatic ␣ cells. Preliminary descriptions of functional glutamate receptors on a  cell line [8] and on isolated islet cells have appeared [9] Such observations raise important questions about the role of glutamate receptors in regulating hormone secretion from islet cells.
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