Striatum plays an important role in the control of motor functions that are dependent on a balance between striatal dopamine and acetylcholine neuromodulators. The main source of acetylcholine in the striatum are cholinergic interneurons (CINs) which express heteromeric nicotinic acetylcholine receptors (nAChRs) containing beta2 subunit (beta2* nAChRs). Our group has previously shown that the deletion of beta2* nAChRs in CINs leads to behavioural changes in mice and to alterations of Fos expression in the striatum. Therefore, we hypothesize that the beta2 deletion leads to a decrease of CINs' activity which in turn leads to an increase of activity in striatal projection neurons. The aim of the current work is to study the effects of beta2 deletion on CINs' firing activity and electrophysiological properties and on local striatal circuits. To this aim, we crossed beta2-flox/flox mice with ChAT(IRES)-Cre mice expressing Cre recombinase selectively in cholinergic neurons. We also characterized the ChAT(IRES)-Cre beta2-flox/flox mice by crossing them with tdTomato reporter line allowing the direct visualization of the CINs. Then we determined passive (membrane resistance and capacitance) and active (electrical excitability) properties of striatal CINs in the control and conditional knock out mice. To investigate possible associations between the electrophysiological changes and behavioural phenotype, we will specifically focus on the analysis of social and anxiety-like behaviour in our mice. The project will help us to evaluate whether targeting beta2* nAChRs expressed by CINs might be used to modulate the CINs' activity and the activity of striatal circuits.