Somatostatin (SST) is a neuropeptide which expression characterizes a subpopulation of GABAergic interneurons. SST exerts its physiological role through 5 G protein-coupled receptors. This neuropeptide is of great interest in the pathophysiological context as a deficit of SST is observed in many neurological diseases, such as epilepsy. In the hippocampus, the effects of SST on the principal cells are known. It inhibits excitatory synaptic transmission by decreasing glutamate release from pyramidal neurons and reduces their intrinsic excitability by facilitating currents carried by Kv7 channels. Within the hippocampus, Oriens - Lacunosum Moleculare interneurons (O-LMs) contain SST and express Kv7.2/3 channels. However, there is no data on the presence of SST auto-receptors on O-LMs, on its mode of release and on the effect SST might have on these interneurons as well as on the modulation of the CA1 feedback circuit. What we observed so far is that O-LMs express SST receptors. Moreover, SST is released by O-LMs following a firing at more than 20Hz and it transiently decreases O-LMs synaptic excitation and excitability but also neighboring pyramidal cells and O-LMs excitability. Thus, exerting both an autocrine and paracrine action on the CA1 feedback circuit. In both cases, this action is mediated by an increase in M current carried by Kv7 channels. Another issue is that SST, once released, is rapidly degraded and its receptors easily internalized, thus precluding the use of SST-based treatments. Using SST Peptide Amphiphiles, we will overcome these problems by creating SST reservoirs, accessible to neurons whenever needed.