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.

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.

God's Organism? The Chick as a Model System for Memory Studies

“…The cartoon of Figure 1 interprets these and the correlative and enhancement data discussed below in terms of a temporal sequence of molecular events in the IMHV following the bead peck. Clements and Bourne (1996); (2) Holscher and Rose (1993); (3) Serrano et al (1994); (4) Clements et al (1995); (5) Crowe et al (1994); (6) Scholey et al (1995); (7) Serrano et al (1994); (8) Mileusnic et al (1996); (9) Mileusnic et al (1999); (10) Freeman and Rose (1995); (11) Holscher and Rose (1994); (12) Rickard et al (1994); (13) Salinska et al (1999); (14) Sandi and Rose (1994b); (15) …”

“…Two in particular are required for longer-term memory-NCAM and neuron/glial CAM (NgCAM) (aka L1) (Scholey et al 1993(Scholey et al , 1995. Both have also been shown to be required for maintenance of LTP (Luthi et al 1994).…”

Multiple cell adhesion molecules shaping a complex nicotinic synapse on neurons

“…Similarly, SynCAM participates in transcellular interactions with other SynCAMs to align pre-and postsynaptic components at glutamatergic synapses (Biederer et al, 2002;Biederer, 2005;Fogel et al, 2007). A third CAM, L1, has also been implicated in synaptic function (Luthl et al, 1994;Scholey et al, 1995;Law et al, 2003;Matsumoto-Miyai et al, 2003;Saghatelyan et al, 2004;Godenschwege et al, 2006). Whether the three CAMs provide largely similar effects or have distinctive roles in synaptogenesis remains unclear.…”

Polysialylated Neural Cell Adhesion Molecule Is Involved in Induction of Long-Term Potentiation and Memory Acquisition and Consolidation in a Fear-Conditioning Paradigm

“…Injections were performed either 2 h after training (Fig. 3A), a time point used previously to study the early phase of consolidation (Doyle et al, 1992;Scholey et al, 1995), or 6 h after train- Figure 1. In vitro LTP recording from the CA1 hippocampal region of NCAM deficient (NCAMϪ/Ϫ) and wild-type (NCAMϩ/ϩ) mice.…”