Involvement of nucleotide diphosphate kinase 2 in the reopening of the sensitive period of filial imprinting of domestic chicks (Gallus gallus domesticus)

Filial imprinting is a behavior characterized by the sensitive or critical period restricted to the first few days after hatching. Once the sensitive period is closed, it is widely believed that chicks can never be imprinted under natural conditions. Previously, we showed that the exogenous injection of T₃ reopened the sensitive period which was already closed. That study suggested that T₃ functioned by way of a rapid non-genomic action; however, the molecular mechanism of how T₃ reopens the sensitive period remains unknown. Here, we show that the phosphorylation level of nucleotide diphosphate kinase 2 (NDPK2) was upregulated following T₃ injection. Pharmacological deprivation of the kinase activity of NDPK hampered the molecular process prerequisite for the reopening of the sensitive period of filial imprinting. Moreover, it is shown that the kinase activity of NDPK2 participates in the priming process by T₃ signaling which endows the potential for learning. Our data indicate that NDPK2 plays a crucial role downstream of T₃ action and that its phosphorylation is involved in the non-genomic signaling during imprinting.