Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002622 (amnesia)
 5,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intraventricular infusions of anti-neural cell adhesion molecule (anti-NCAM) are demonstrated to inhibit consolidation of a passive avoidance response when administered in the 6-8 h posttraining period. Anti-NCAM was ineffective when administered during training or at any other time up to 10 h thereafter, and no amnesic effects were observed with absorbed anti-NCAM or anti-neurofilament protein. Amnesia was observed only at the 48-h recall time, and this could not be attributed to poor antibody penetration or a prolonged residence time, as studies with 125I-labelled anti-NCAM in trained animals demonstrated a rapid accumulation into all brain regions, and this was marked in the olfactory bulb and hippocampus, areas showing an inherent and paradigm-specific increase in NCAM sialylation state, respectively. The lack of an amnesic action at the 24-h recall time is attributed to anti-NCAM-impaired synapse structuring becoming apparent following the paradigm-specific increases in NCAM sialylation state.
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PMID:Intraventricular infusions of anti-neural cell adhesion molecules in a discrete posttraining period impair consolidation of a passive avoidance response in the rat. 140 6

One-trial passive avoidance training in day-old chicks results in a biochemical cascade occurring in two forebrain regions, the intermediate medial hyperstriatum ventrale and the lobus parolfactorius. This cascade, initiated by synaptic transients, results in the activation of immediate early genes and culminates in the de novo synthesis of a family of pre- and post-synaptic membrane glycoproteins, that, inserted into the membrane, serve in the remodelling of synaptic connectivity which is a requirement for the brain representations constituting long-term memory. There are two waves of glycoprotein synthesis consequent on training, the first occurring within an hour of the training experience and the second 5.5-8 h post-training. Blocking synthesis during these time windows results in amnesia for the task. Amongst the glycoproteins involved are two cell adhesion molecules, NCAM and L1. Injection of antibodies to L1 result in amnesia if injected during either time window, but not outside these times; antibodies to NCAM result in amnesia only if injected at the 5.5-h timepoint. I interpret these results as indicating that de novo synthesis of NCAM during the second time window is necessary for producing a persistent memory trace.
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PMID:Glycoproteins and memory formation. 775 3

Polyclonal antibody R-1, raised against a chick synaptic membrane glycoprotein fraction whose synthesis is enhanced following training on a passive avoidance task, produces amnesia when injected into chick forebrain 5.5 h posttraining. The amnestic IgG fraction specifically recognizes a low sialylated isoform of NCAM (Mileusnic Rose, Lancashire, & Bullock, 1995). We have now investigated the effects of this antibody on memory formation in adult rats. R-1, preimmune serum, or saline was injected intracerebroventricularly 5.5 h posttraining through bilaterally implanted cannulae. Rats injected with R-1 and tested 48 h later showed a significant amnesia for avoidance compared with the controls. Amnesia was not apparent at 24 h posttraining. R-1 injections were without effect on spontaneous locomotor or exploratory activity in a holeboard test. The results contribute to the argument that the role of cell adhesion molecules in neuronal plasticity is not limited to the developing nervous system, but they play a more general role in the experience-dependent synaptic remodeling underlying long-term memory.
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PMID:Antibody to day-old chick brain glycoprotein produces amnesia in adult rats. 901 96

The functional role of NCAM gene expression in memory formation was studied in the one-trial passive avoidance task in day-old chicks by pretraining injections of one of three different 18-mer end-protected oligonucleotides corresponding to positions 190-, 207-, and 332- of the NCAM Ig1 domain. Twenty-four-hour-old chicks were trained by pecking at a bitter-tasting bead and tested for avoidance 30 min, 3, 8, or 24 hr later. Memory retention was significantly reduced only in the group of animals injected with the NCAM antisense corresponding to position 207- (AS-ODN-207), and only if given twice, both immediately after hatching and 12 hr before training. This antisense was without effect on the general behavior of the chicks, training or acquisition, and did not produce observable neurotoxic damage. Under such conditions amnesia was evident by 3 hr after training and lasted until at least 24 hr after training. The two other tested oligonucleotides were without behavioral effect. To control for nonsequence-specific effects of AS-ODN-207, brains from injected and trained animals were processed for Western blotting and probed using anti-NCAM, anti-L1, and anti-actin antibodies. NCAM antisense corresponding to position 207- significantly reduced the level of NCAM, whereas the level of L1 and actin remained unchanged. These results confirm our earlier conclusion that NCAM is necessary for longer term memory retention.
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PMID:Sequence-specific impairment of memory formation by NCAM antisense oligonucleotides. 1032 37