Resumo

Neuronal calcium sensor-1 (NCS-1) is a member of the neuronal calcium sensor protein subfamily and is highly conserved throughout evolution, with orthologs identified from yeast to humans. NCS-1 plays a role in neuronal plasticity, regulating neurotransmitter release, long-term synapse modification, receptors and ion channels. Here, we focus on the initial characterization of NCS-1 knockout (KO) mice in a C57BL/6 background. NCS-1 KO mice are viable and do not display any detectable morphological disturbance. In contrast, assessing their behavior phenotype, a lack of NCS-1 is enough to cause anxious and depressive-like behavior, observed in the forced swim test and elevated plus-maze, respectively. Anxious and depressive-like behaviors were reversed by the anxiolytic drug diazepam and the antidepressant drug imipramine, respectively, resembling the WT phenotype treated with the same drugs. Furthermore, nonaversive long-term memory was impaired in NCS-1 KO mice, as demonstrated by spontaneous object recognition test. Therefore, NCS-1 appears to regulate brain function in a complex mammal model system, and its disruption causes a disorder of the behavior output phenotype.