Acute stress and dexamethasone rapidly increase hippocampal somatostatin synthesis and release from the dentate gyrus hilus

AbstractSomatostatin is a neuropeptide whose facilitatory action in the generation of long‐term potentiation (LTP) in the hippocampal dentate gyrus has been associated with memory processes. Since stress and memory seem to share some neural pathways, we studied somatostatin release from dentate gyrus hilar cells of the hippocampus in unanesthetized free‐moving rats subjected to stress or dexamethasone treatments. In parallel, the number of dentate gyrus hilar cells expressing somatostatin mRNA was quantified by nonradioactive in situ hybridization in these two experimental conditions.Rats were stereotaxically implanted with a push‐pull cannula in the dentate gyrus hilar region. Animals were perfused 1 week later in basal or stress (30 min immobilization stress) conditions. The other group was intraperitoneally injected with the synthetic glucocorticoid dexamethasone (3 mg/kg b.w.). Samples were collected every 15 min for somatostatin radioimmunoassay. In parallel, in other groups of animals undergoing the same treatments, brains were removed for in situ hybridization studies with an oligonucleotide labeled with digoxigenin that recognizes somatostatin‐14.The results showed that stress induced a significant increase in somatostatin release from dentate gyrus hilar cells 30–45 min after immobilization stress application. Dexamethasone‐injected animals exhibited a similar response 45 min after drug administration. In situ hybridization analysis revealed that the two treatments significantly increased the number of cells expressing somatostatin mRNA in the hilar region.In conclusion, somatostatin interneurons of the hippocampal hilar region appear to be a novel stress stimulus target. Their rapid reactivity, expressed as modifications of both somatostatin release and number of cells expressing somatostatin mRNA, provides an interesting model of neuronal plasticity. Hippocampus 2001;11:469–477. © 2001 Wiley‐Liss, Inc.