Abstract
To investigate the involvement of the cell adhesion molecules L1.1, L1.2, NCAM, and tenascin‐C in memory formation, zebrafish (Brachydanio rerio) were trained in an active avoidance paradigm to cross a hurdle to avoid mild electric shocks after a light signal. Application of [14C]deoxyglucose prior to the training session revealed an increased energy demand in the optic tectum during acquisition of the active avoidance response compared with untrained fish and with fish not learning the task (nonlearners). In situ hybridization with digoxigenin‐labeled cRNA probes directed against zebrafish L1.1, L1.2, NCAM, and tenascin‐C revealed an enhanced expression of L1.1 and NCAM mRNA in the optic tectum of learners 3 h after acquisition of the task compared with untrained fish, nonlearners, overtrained fish, and learners decapitated 1 or 6 h after acquisition. Levels of L1.2 mRNA were not significantly increased in the tectum 3 h after learning. Tenascin‐C was neither expressed in the optic tectum of untrained fish nor in the tectum of learners. To test for a possible involvement of L1.1 in memory consolidation, antibodies were injected intracerebroventricularly 1 h after the last training trial. Two days later, injected zebrafish were tested for recall and evaluated by a retention score (RS), ranging from 1.0 for immediate recall to 0.0 indicating no savings. The average retention score of L1.1 antibody‐injected fish (RS = 0.29) was different from that of tenascin‐C antibody‐injected (RS = 0.71) or uninjected fish (RS = 0.78), indicating a pivotal function of L1.1 in long‐term memory formation in zebrafish. © 2000 John Wiley & Sons, Inc. J Neurobiol 43: 389–403, 2000