LNX1 and LNX2 proteins are closely related PDZ domain-containing E3 ubiquitin ligases expressed in neurons. They can interact with and potentially modulate a numerous synaptic proteins, but the in vivo physiological relevance of most of these interactions remains uncertain. We previously reported that mice lacking both LNX1 and LNX2 in the central nervous system exhibit decreased anxiety-related behaviour. Separately, abnormalities in social learning and sociability were described in a distinct LNX1 knockout mouse line. To extend this work we have examined: (1) anxiety-related behaviour in LNX1 and LNX2 single knockout animals, (2) social learning and sociability in LNX2 single knockout and LNX1/LNX2 double knockout mice for the first time and (3) additional anxiety-related behaviours in LNX knockout mice including the emergence, marble burying and ultrasonic vocalization tests. In addition, abnormalities in hippocampal circuitry and synapse maturation previously associated with social learning deficits have been examined in our distinct LNX1 knockout line, as well as in LNX2 knockout animals. Results of behavioural tests suggest that both LNX1 and LNX2 contribute to the decreased anxiety-related behaviour previously seen in double knockout mice. Our data also points towards a previously unappreciated involvement of LNX2 in sociability and social learning. Certain aspects of previously reported hippocampal circuitry defects are recapitulated in our LNX1 knockout mice and a comparative analysis made in LNX2 knockout animals. These results provide novel insights into the functions of the enigmatic LNX proteins in the brain and their potential involvement in behaviours of relevance to anxiety and autism spectrum disorders.