contrast, a study using autaptic hippocampal cultures derived from a different APP KO mouse line showed an increase in synaptophysin-immunoreactive puncta and miniature synaptic currents (Priller et al., 2006). These conflicting results are compounded by APLP1 and APLP2, which likely play redundant functions that compensate for the loss of APP in the intact animal. However, more recent studies in double APP/APLP2-deficient, but not single APP KO, animals have clearly identified developmental defects in neuromuscular junction synapses with corresponding neurophysiological deficits (Wang et al., 2005). Thus, the situation with single APP KO mice remains unresolved.
