EN
Autism is a multifactorial disorder that involves impairments in social interactions and communication, as well as restricted and repetitive behaviors. Recent whole-genome exon sequencing studies of ASD (autism spectrum disorders) samples estimate that as many as 100 to 1 000 genes may be involved. So different candidate genes have been tested in mouse models by knocking them out. Calbindin D-28k (CB) and parvalbumin (PV) are cytosolic calcium-binding proteins expressed in many neurons without general preference for functionally and morphologically defined subpopulations. Deletion of CB and/or PV alters intracellular calcium signaling, and physiological properties of affected neurons. General knockouts for both proteins display a distinct and permanent motor impairment which is revealed only when adaptation of movement to novel environmental conditions is required. In order to determine whether the absence of CB and PV influences locomotor properties and behavior we compared mouse lacking CB, PV, or both with wild type controls. The mice were compared in the open field task and in the light-dark compartment tests to measure activity, exploratory behavior, and restricted and repetitive behaviors (TruScan, Coulbourn, USA). Relative to wild-type mice, the transgenic mice exhibited much more stereotypic movements in the open field test. Multiple mouse behavioral effects suggest that the CB and PV genes may play a role in modulating behaviors relevant to psychiatric disorders.