Changes in excitability of excitatory neurons, as well as strengthening of excitatory synapses, have been postulated to underlie learning and memory mecha‑ nisms. The GABAergic system is also plastic, however, the mechanisms of plasticity in inhibitory systems are poorly understood, especially considering the diverse nature of inhibitory interneurons. There are three main groups of inhibitory interneurons in the neocortex: so‑ matostatin (SOM)-, parvalbumin (PV)-, and vasoactive intestinal polypeptide (VIP)-expressing interneurons. The aim of our study is to analyse the effect of learning on the activity of SOM-expressing interneurons, which have been implicated in state-dependent modulation and experience-dependent plasticity, and with activity regulated by neuromodulators. In our experiments, we used a simple model of sensory learning, where mice were subjected to a conditioning paradigm ingthat con‑ sisted of pairing tactile stimulation of whiskers with an electrical tail shock. Previous studies have shown that this paradigm results in an expansion of the cortical rep‑ resentation of stimulated vibrissae and in an increase in GABAergic transmission. Here, using transgenic mice with SOM interneurons genetically tagged with red fluorescent marker, we performed in vitro whole-cell patch-clamp recordings in slices of naïve and trained mice. We analysed basic electrophysiological properties and excitability of SOM cells located in layer IV of the representation of the “trained” whiskers in the barrel cortex. In addition, spontaneous excitatory (sEPSCs) and inhibitory (sIPSCs) postsynaptic currents in SOM cells were recorded. In agreement with the literature, we found two main groups of SOM interneurons in lay‑ er 4: low-threshold spiking and irregular spiking. After the learning paradigm, the excitability of low-threshold spiking SOM interneurons increased. There were no dif‑ ferences in either the amplitude or the frequency of sEP‑ SCs (and IPSCs) in SOM cells between groups. These data indicate that sensory training results in a selective and long-lasting enhancement of SOM interneuron activity due to changes in their intrinsic excitability. Hence, this study builds upon a growing body of literature suggest‑ ing that increases in inhibition are a common and im‑ portant mechanism of learning and memory.