Abstract
During development of the nervous system, molecular signals mediating cell-cell interactions play critical roles in the guidance of axonal growth and establishment of synaptic functions. The Eph family of tyrosine kinase receptors and their ephrin ligands has been shown to mediate neuronal interactions in the development of topographic axon projection maps in several brain regions, and the loss of Eph activities result in defects in select axonal pathways. However, effects of deficiencies of the Eph signals on animal behavior have not been well documented. In this study, we showed that inactivation of a ligand of the Eph receptors, ephrin-A5, resulted in defects in maternal behavior and alterations in anxiety. Female ephrin-A5 -/- mice show significant defects in nest building and pup retrieval. In addition, lower levels of anxiety were observed in both male and female null mice. These changes were not due to deficiencies in estradiol, progesterone or corticosterone levels. Our observations suggest that ephrin-A5 plays a key role in the development and/or function of neural pathways mediating mouse maternal care and anxiety.
Highlights
Proper maternal behavior is essential for survival of the offspring (Numan & Insel, 2003)
There were no significant differences in nest score between the genotypes at all three time points suggesting that ephrin-A5 deletion does not affect the motor ability of the mice to build a non-maternal nest
We demonstrate that genetic deletion of ephrin-A5 significantly decreased maternal behavior
Summary
Proper maternal behavior is essential for survival of the offspring (Numan & Insel, 2003). Shoji et al (Shoji & Kato, 2009) compared the maternal behavior of the offspring of two inbred mice, CBA/Ca and BALB/c, which differ in their levels of maternal care; CBA/Ca females exhibit nursing and pup licking more frequently and retrieve their pups faster than BALB/c females. They found that low levels of maternal care earlier in life (by BALB/c dams) decreased maternal behavior in the offspring
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