Information processing within neural networks is determined by a dynamic partnership between principal neurons and local circuit inhibitory interneurons. GABAergic interneurons represent the dominant inhibitory cell type throughout the mammalian central nervous system. This population of neurons is extremely heterogeneous and comprises, in many brain regions, cells with divergent morphological and physiological properties and highly specialized functions.
During the past two decades, GABAergic inhibitory interneurons have been studied extensively, especially in the hippocampus, a relatively simple cortical structure. Different types of hippocampal inhibitory interneurons control the spike initiation (e.g., axo-axonic and basket cells) and synaptic integration [e.g., bistratified and oriens-lacunosum moleculare (O-LM) interneurons] within pyramidal neurons and synchronize local network activity, providing a means for functional segregation of neuronal ensembles and proper routing of hippocampal information.
Thus, it is thought that, at least in the hippocampus, GABAergic inhibitory interneurons represent critical regulating elements at all stages of information processing, from synaptic integration and spike generation to large-scale network activity. However, it remains largely unknown what cellular and molecular mechanisms control the activity of inhibitory interneurons themselves.
In search of answer to this fundamental question, we use a combination of two-photon laser scanning microscopy, whole-cell patch clamp electrophysiology, optogenetics, single-cell transcriptomics, pharmacogenetics, immunohistochemistry, electron microscopy and genetic approaches in brain slices and in behaving mice. An emphasis is placed on the examining of the inhibitory control of inhibitory interneurons and interneuron dendritic integration.
Current research program encompasses two themes:
• Cellular Basis of Synaptic Communications between Inhibitory Interneurons in the Hippocampus with a focus on VIP-expressing interneuron-selective cells;
• Dendritic integration and synaptic plasticity in inhibitory interneurons.