Altered motor activity and social behavior in zebrafish lacking the Hcn2b ion channel

HCN channels are widely expressed in the brain and heart where they contribute to a variety of functions, including pacemakers, control of rhythmic firing, regulation of neuronal excitability and synaptic plasticity. Here, using zebrafish Danio rerio, we describe the brain and heart expression of hcn2b mRNA, the orthologous gene of human HCN2, and show that a loss of function of the hcn2b gene is associated with a slight, though not statistically significant, increase in basal electrical brain activity and fosab expression. We demonstrate that hcn2b mutants increase motor activity during the day-cycle and show social aversion. Our findings provide evidence that lack of Hcn2b channel function affects social behavior, supporting its relevance as a zebrafish model for studying HCN2-related neurological disorders.