These results suggest that limited brain sites, mainly the hippocampus and cerebellum, might contribute to the dominant phenotype, spatial learning impairment and motor discoordination in ADAM11-deficient mice. In situ hybridisation analysis has detected Adam11 gene expression in the pyramidal cells of CA1–CA3 fields and granule cells of the dentate gyrus in the hippocampus and in granular cells in the cerebellum [25]. It is unlikely that morphological changes during development led to impairment of spatial learning and motor coordination, and morphological alterations in the cytoarchitecture of the hippocampus and cerebellum were not observed in ADAM11-deficient mice after histological investigation using HE staining. However, because it is thought that ADAM11 plays a role in neuron-neuron or neuron-glial cell interactions, a more precise morphological investigation will be needed. It has been reported that adhesion molecules, such as neural cell adhesion molecule (NCAM), are not only implicated in cell interactions during nervous system development, but are also recognised as important mediators of synaptic plasticity in the adult nervous system [35]. Changes in neuron excitability in the hippocampus, such as decreases in the post-burst after hyperpolarization (AHP), have been thought to affect long-term potentiation (LTP) [36], an experimental model of the synaptic changes thought to underlie learning and memory [37]. It has also been reported that mice lacking NMDA receptor for both NR2A and NR2C subunits showed motor dysfunction and complete loss of both spontaneous and evoked excitatory postsynaptic currents (EPSCs) in cerebellar granule cells [38]. Therefore, electrophyological studies to enable analysis of synaptic transmission and plasticity in the hippocampus and cerebellum of ADAM11-deficient mice will be needed. These studies might clarify whether ADAM11 plays an important signalling or structural role at the synaptic level and whether it participates in synaptic regulation.