A role for a chicken homolog of the neural cell adhesion molecule L1 in consolidation of memory for a passive avoidance task in the chick.

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Abstract
Intracranial injection of antibodies directed against the neural cell adhesion molecule L1 resulted in amnesia for passive avoidance training in day-old chicks tested 24 hr subsequently. L1 antibodies were amnesic when administered at one of two time windows: 30 min pretraining and 5.5-8 hr post-training. No amnesia was apparent if injections were made at times before, between, or after these time windows (-2, +1, +3, +4, or +12 hr relative to training). A fragment of the L1 molecule derived from the external fibronectin domains FN1-5 produced amnesia only when injected at the 5.5-hr timepoint, whereas a fragment of the immunoglubin-like domains Ig I-VI produced amnesia only when injected 30 min prior to training. We have shown previously that long-term memory for the passive avoidance task requires two waves of glycoprotein synthesis, the first occurring immediately after training, and the second some 6 hr thereafter. The glycoprotein synthesis inhibitor 2-deoxygalactose results in amnesia if injected at either time, whereas the neural cell adhesion molecule (N-CAM) is specifically involved only in the second wave. The coincidence of the time course of memory disruption resulting from injection of L1 antibodies with that occurring with 2-deoxygalactose supports the hypothesis that establishment of an enduring memory for the experience of passive avoidance training requires two waves of glycoprotein synthesis, each wave being biochemically and functionally discrete. The differential effects of the two L1 fragments suggests that separate mechanisms of synaptic stabilization are involved at the two time points.

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