Long-term potentiation in mice lacking the neural cell adhesion molecule L1

Genetic evidence indicates that cell adhesion molecules of the immunoglobul in superfamily (IgCAMs) are critical for activity dependent synapse formati on at the neuromuscular junction in Drosophila and have also been implicate d in synaptic remodelling during learning in Aplysia (see [1] for review). In mammals, a widely adopted model for the process of learning at the cellu lar level is long term potentiation (LTP) in the hippocampal formation. Stu dies in vitro have shown that antibodies to the IgCAMs L1 and NCAM reduce L TP in CA1 neurons of rat hippocampus, suggesting a role for these molecules in the modulation of synaptic efficacy, perhaps by regulating synaptic rem odelling [2]. A role for NCAM in LTP has been confirmed in mice lacking NCA M [3] (but see [4]), but similar studies have not been reported for L1. Her e we examine LTP in the hippocampus of mice lacking L1 [5,6], using differe nt experimental protocols in three different laboratories. In tests of LTP in vitro and in vivo we found no significant differences between mutant ani mals and controls, Thus, contrary to expectation, our data suggest that L1 function is not necessary for the establishment or maintenance of LTP in th e hippocampus. Impaired performance in spatial learning exhibited by L1 mut ants may therefore not be due to hippocampal dysfunction [6].