TY - JOUR T1 - Decreased Anxiety, Altered Place Learning, and Increased CA1 Basal Excitatory Synaptic Transmission in Mice with Conditional Ablation of the Neural Cell Adhesion Molecule L1 JF - The Journal of Neuroscience JO - J. Neurosci. SP - 10419 LP - 10432 DO - 10.1523/JNEUROSCI.23-32-10419.2003 VL - 23 IS - 32 AU - Janice W. S. Law AU - Alan Y. W. Lee AU - Mu Sun AU - Alexander G. Nikonenko AU - Sookja K. Chung AU - Alexander Dityatev AU - Melitta Schachner AU - Fabio Morellini Y1 - 2003/11/12 UR - http://www.jneurosci.org/content/23/32/10419.abstract N2 - L1, a neural cell adhesion molecule of the immunoglobulin superfamily, is involved in neuronal migration and differentiation and axon outgrowth and guidance. Mutations in the human and mouse L1 gene result in similarly severe neurological abnormalities. To dissociate the functional roles of L1 in the adult brain from developmental abnormalities, we have generated a mutant in which the L1 gene is inactivated by cre-recombinase under the control of the calcium/calmodulin-dependent kinase II promoter. This mutant (L1fy+) did not show the overt morphological and behavioral abnormalities observed previously in constitutive L1-deficient (L1-/-) mice; however, there was an increase in basal excitatory synaptic transmission that was not apparent in L1-/- mice. Similar to L1-/- mice, no defects in short- and long-term potentiation in the CA1 region of the hippocampus were observed. Interestingly, L1fy+ mice showed decreased anxiety in the open field and elevated plus-maze, contrary to L1-/- mice, and altered place learning in the water maze, similar to L1-/- mice. Thus, mice conditionally deficient in L1 expression in the adult brain share some abnormalities, but also display different ones, as compared with L1-/- mice, highlighting the role of L1 in the regulation of synaptic transmission and behavior in adulthood. ER -