INTRODUCTION: Cortical interneurons containing somatostatin (SST-INs) are the second most numerous subtype of GABA-ergic cells in the somatosenory cortex of rodents. SST‑INs inhibit excitatory cells and also other inhibitory interneurons. They are involved in disinhibitory circuits, in which SST-INs inhibit interneurons containing parvalbumin (PV-INs) which, in turn, stop inhibiting excitatory neurons. Somatostatin is present in synapses in a separate pool of vesicles and may be released together with GABA. Activation of somatostatin receptors in the brain may cause inhibition of adenylyl cyclase, decrease of intracellular Ca2+ levels, hyperpolarization of cells mediated by K+ channels, protein phosphatases activation and MAP kinases modulation. Somatostatin action on PV‑INs is poorly understood. AIM(S): To get a picture of possible sites of somatostatin action upon PV-INs, we examined the distribution of five subtypes of somatostatin receptors (SSTRs1‑5) on genetically labeled PV‑INs in the barrel cortex. METHOD(S): The experiment was conducted on PV‑ires‑Cre driver mice lines crossed with the Ai14 line to obtain tdTomato expression following Cre-mediated recombination. Cre‑dependent cell labeling was verified by immunocytochemical reaction with anti-PV antibody. A series of immunofluorescent staining using antibodies against SSTR1‑5 were performed on coronal and tangential brain sections. RESULTS: We found that SSTR1, SSTR3, and SSTR5 were present on PV‑INs in all cortical layers (74% to 96% of PV neurons showed colocalization with these SSTRs). SSTR4 was found only on 36% to 62% of PV neurons, depending on the layer. Immunolabeling was found on cell bodies and dendrites. Surprisingly, we did not observe SSTR2 presence on PV‑INs in any cortical layer. CONCLUSION: Apparently, somatostatin acts on PV-INs through only four receptor subtypes, excluding SSTR2. FINANCIAL SUPPORT: Supported by National Science Center grant OPUS 2015/17B/NZ/02016 to MK.