GABAergic inhibitory interneurons (INs) in the mammalian cortex are characterized by a broad diversity based on their molecular, morphological and physiological characteristics. The various IN types are thought to control the activity and  excitability of their target cells in a compartment-specific manner. Recent investigations in our group indicate that some IN types are under plasticity control. In our research we focus on the mechanisms that allow long term strengthening or weakening of glutamatergic synaptic inputs onto parvalbumine (PV) and somatostatin (SOM)-expressing interneurons (PVIs, SOMIs, respectively). We aim to understand how these synaptic plastic changes contribute to the overall state of the neural network activity in which these INs are embedded in, information processing and the behavior output. To accomplish these aims, we use a multidisciplinary approach combining in vitro whole-cell recordings, shRNA for interference with synaptic plasticity induction, in vivo single unit recordings of optotagged IN types and behavioral analysis. We focus these investigations on PVIs and SOMIs of the dentate gyrus in mice. We previously showed that mossy fiber synapses originating from dentate gyrus granule cells mediate long-term potentiation (LTP) onto both IN types. This form of LTP depends on the activation of group I metabotropic glutamate receptors (Sambandan et al., J Neurosci 2010; Hainmueller & Bartos, PNAS USA 2014; Yuan et al., eLife 2017).



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