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Glutamate Pathways Mediate Somatostain Responses to Glucose in Normal and Diabetic Rat Hypothalamus
Author(s) -
; Lewis,
' Ham,
William Scanlon
Publication year - 1998
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1046/j.1365-2826.1998.00218.x
Subject(s) - kainate receptor , medicine , endocrinology , metabotropic glutamate receptor , ionotropic effect , glutamate receptor , ampa receptor , chemistry , metabotropic receptor , somatostatin , metabotropic glutamate receptor 5 , biology , receptor
We investigated the role of hypothalamic glutamate receptors in mediating the stimulatory effect of low glucose (<5 mM) on somatostatin release. We also studied whether alteration in glutamate release might contribute to the reduced hypothalamic somatostatin response to low glucose observed in diabetic (Goto‐Kakizaki) rat hypothalami. Hypothalamic somatostatin release in response to incubation with 1 mM d ‐glucose was inhibited by the ionotropic glutamate receptor antagonists MK801, D‐AP5 and DNQX but not by the metabotropic antagonists L‐AP3 or MCPG. The release of somatostatin was increased by the ionotropic agonists NMDA, AMPA and kainate but not by metabotropic agonists t‐ACPD or L‐AP4. Basal and peak glutamate release in response to incubation with 1 mM glucose, were significantly lower from GK hypothalami There were no significant differences in the basal or stimulated release of serine and GABA. These data indicate that ionotropic NMDA/AMPA/kainate receptors and not metabotropic receptors mediate the effects of glucose on rat hypothalamic somatostatin release. Reduced hypothalamic somatostatin release in response to low glucose in diabetic (Goto‐Kakizaki) rats may well be secondary, at least in part, to reduced glutamate release.