Glutamate Pathways Mediate Somatostain Responses to Glucose in Normal and Diabetic Rat Hypothalamus
| Autor: | B G, Issa, B M, Lewis, J, Ham, J R, Peters, M F, Scanlon |
|---|---|
| Rok vydání: | 1998 |
| Předmět: |
endocrine system
medicine.medical_specialty Endocrinology Diabetes and Metabolism Hypothalamus Glutamic Acid Kainate receptor AMPA receptor Cellular and Molecular Neuroscience Endocrinology Reference Values Internal medicine Diabetes Mellitus Excitatory Amino Acid Agonists medicine Animals Amino Acids Rats Wistar Endocrine and Autonomic Systems Metabotropic glutamate receptor 5 Chemistry Metabotropic glutamate receptor 6 Rats Inbred Strains Rats Glucose Somatostatin Metabotropic receptor Metabotropic glutamate receptor NMDA receptor Excitatory Amino Acid Antagonists hormones hormone substitutes and hormone antagonists |
| Zdroj: | Journal of Neuroendocrinology. 10:377-381 |
| ISSN: | 1365-2826 0953-8194 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|