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)

Training chicks on a one-trial passive avoidance task results in a cellular cascade over the subsequent hours. Phosphorylation of the presynaptic phosphokinase C substrate B-50 is followed by immediate-early gene expression and increased synthesis of pre- and postsynaptic glycoproteins, increases in dendritic spine densities, synapse and synaptic vesicle numbers, and a prolonged increase in neuronal bursting. Many of these effects have been localized to two forebrain regions: the left intermediate medial hyperstriatum ventrale and the lobus parolfactorius. Pretraining lesions in the left intermediate medial hyperstriatum ventrale, or post-training lesions in the lobus parolfactorius result in amnesia. These and related results lead to models of memory storage based on multiple representation by way of synaptic stabilization through glycoprotein synaptic recognition molecules.
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PMID:How chicks make memories: the cellular cascade from c-fos to dendritic remodelling. 172 May 78

2-Deoxy-D-galactose, an inhibitor of brain glycoprotein fucosylation, was injected intracranially (10 mumole dose in 10 microliters) into either the left or the right forebrain hemisphere of day-old chicks (Gallus domesticus). Bilateral injection of this dose of 2-deoxy-D-galactose is known to induce amnesia for several learning tasks including one-trial passive avoidance and sickness-induced learning. When a tritiated form of the drug was injected into one forebrain hemisphere only, a significantly large proportion of the dose remained in that hemisphere. Chicks were trained in two different one-trial learning tasks. The first was a passive avoidance task in which the chicks were allowed to peck at a green training stimulus (a small light-emitting diode, LED) coated in the bitter liquid, methylanthranilate, giving rise to a strong disgust response and consequent avoidance of the green stimulus. In the second paradigm the chicks were allowed to peck at a similarly colored dry stimulus but, 30 min later, were injected intraperitoneally with lithium chloride (0.1 ml of 1 M solution), causing a sickness-induced aversion for the green LED. 2-Deoxy-D-galactose caused amnesia for the passive avoidance task when injected before training into the right hemisphere but not the left. However, unilateral injection of the drug before training on the sickness-induced learning task did not cause amnesia. The results indicate that fucosylation of brain glycoproteins is required in the right hemisphere for learning the passive avoidance task but that memory for sickness-induced learning can be retained by either hemisphere.
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PMID:Amnesia induced by 2-deoxygalactose in the day-old chick: lateralization of effects in two different one-trial learning tasks. 186 28

Ependymins are acidic glycoprotein constituents of goldfish brain cytoplasm and extracellular fluid which are known to participate in biochemical reactions of long-term memory formation. In earlier experiments, anti-ependymin antisera were found to cause amnesia when injected into goldfish brain ventricles after the acquisition of a vestibulomotoric training task. To investigate whether they also inhibit memory consolidation after other learning events the anti-ependymin antisera were injected after an active shock-avoidance learning paradigm, as follows: goldfish were trained in a shuttle-box to cross a barrier in order to avoid electric shocks (unconditioned stimulus) applied shortly after a light signal (conditioned stimulus). Anti-ependymin antisera blocked retention of the learned avoidance when injected 0.5, 4.5 or 24 h after acquisition of the new behavior. They had no effect, however, when injected 72 h after learning. Apparently, long-term memory was already consolidated at this point. Antisera injected 0.5 or 72 h prior to training, also did not influence learning or memory. Thirteen percent of the goldfish fled the light stimulus spontaneously. These fish therefore did not experience the unconditioned stimulus and thus were unable to learn the task. When they were treated with the anti-ependymin antisera and tested 3 days later, the spontaneous escape reaction was not affected (active control group). The ability of anti-ependymin antisera to inhibit memory consolidation and their efficacy after administration at specific time intervals are very similar for the active shock-avoidance learning and for the vestibulomotoric training. We conclude that ependymins are not task-specific, but serve a general function in biochemical reactions essential for long-term memory formation.
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PMID:Inhibition of long-term memory formation by anti-ependymin antisera after active shock-avoidance learning in goldfish. 335 56

Colchicine, injected bilaterally into the forebrain of day-old chicks at times before and after one-trial avoidance learning, produced transient amnesia for one to three hours after learning, that could not be accounted for as a perceptual or attentional defect. The amnesia was dose dependent and was produced only when injections occurred within a limited period before and after learning. No amnesia occurred when injections were given 120 min before or 60 min later than the learning trial, nor at times prior to the retrieval test. During the amnesic period, new learning could occur and be retrieved 15 min later. The amnesia could be overcome by retention-testing or by a new, related, learning experience before or up to 30 min after onset of amnesia. Control birds injected with saline or lumicolchicine, a biologically inactive derivative of colchicine, showed normal retention. Vinblastine sulphate, which also interrupts microtubular networks and hence axonal flow, had no amnesic properties. Colchicine injections had no effect on the levels of acetylcholinesterase, choline acetyltransferase, glutamic acid decarboxylase, and muscarinic acetylcholine receptors in the whole forebrain or in forebrain synaptosomes during the amnesic period. Nor did colchicine injections affect amino acid uptake and protein or glycoprotein synthesis before or during the amnesic period, although there was 10-20% inhibition of protein synthesis 5 h after injection. Thus over the amnesic period, there was no evidence of gross perturbation of brain function. Electron microscopy showed microtubules intact within 1 mm of the injection site 2.5 after injection. Oedema was found at this time in chicks injected with a high dose (100 micrograms) shown to disturb behaviour grossly, but not with a low dose (5 micrograms) which caused amnesia. Transient amnesia for one-trial avoidance learning is most probably caused by secondary effects of colchicine on nerve cell function. We suggest that the amnesic episode represents destruction of one of the stages of a multiple independent parallel process of memory consolidation.
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PMID:The effects of colchicine and vinblastine on memory in chicks. 616 77

Antisera were prepared against six postsynaptic density glycoprotein fractions (150-180, 62-80, 50, 41, 33, and 28 kDa) that show enhanced fucosylation during memory formation after training day-old chicks in a one-trial passive avoidance task. Each antiserum was tested for its possible effect on memory retention. Bilateral intracranial injections of two of the antisera, R-1 and R-6, or their IgGs (IgG-1 and IgG-6), resulted in amnesia for the passive avoidance task when chicks were tested 24 h later, IgG-1 and IgG-6 antibodies were amnestic only when injected 5.5 h after training, and had no effect when injections were made 30 min before training, thus resembling an effect previously observed with polyclonal or monoclonal anti-N-CAM antibodies. IgG-1 and IgG-6 antibodies were found to be specific for protein epitopes of glycoproteins that contain a high amount of N-linked mannose and fucose, and a very low amount of polysialic acid and O-linked galactose. Absorption of IgG-6 antibodies with neural cell adhesion molecule (N-CAM) isolated from synaptic plasma membranes derived from day-old chick brain resulted in loss of amnestic effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Characterisation of antibodies specific for chick brain neural cell adhesion molecules which cause amnesia for a passive avoidance task. 753 55

The antibiotic anisomycin (ANI), a protein synthesis inhibitor, was used to investigate the time-related changes in protein synthesis following passive avoidance training in the day-old chick. Retention of memory for this simple learning task is known to be prevented by protein synthesis inhibitors within the first hour post-training. Here we report a second, later time window during which inhibition of protein synthesis results in amnesia following one-trial passive avoidance training. Birds were given bilateral intracranial injections of ANI (10 microliters/hemisphere of a 30 mM solution) at various times relative to training and tested 24 h later. Injections given between 0.5 h prior to 1.5 h post-training or 4-5 h post-training, but not at later or at intervening times, resulted in amnesia. These results are discussed in the context of earlier findings, using the inhibitor of glycoprotein synthesis 2-deoxygalactose, that memory formation shows two glycoprotein-synthesis-dependent periods of sensitivity (Scholey, Rose, Zamani, Bock, & Schachner, 1993). The time windows of susceptibility of ANI and 2-Dgal are consistent with a model in which there are two waves of neural activity following training; during the second, commencing 4 h after training, proteins are synthesized and then glycosylated as part of the establishment of an enduring memory trace.
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PMID:Two time windows of anisomycin-induced amnesia for passive avoidance training in the day-old chick. 767 Aug 43

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

The effect of 2-deoxygalactose (2-D-gal), an inhibitor of glycoprotein synthesis, on memory formation was investigated with the day-old chick trained on a single-trial passive discrimination task. 2-D-gal (10 mumol/chick) was shown to inhibit memory formation at a time before the emergence of an antibiotic-sensitive long-term memory stage. The amnestic effect of 2-D-gal was successfully prevented by galactose, and more significantly by noradrenaline. In contrast, anisomycin-induced amnesia was resistant to challenge by either galactose or noradrenaline. The results are consistent with the view that some glycoprotein involvement in memory formation occurs prior to the formation of protein synthesis-dependent long-term memory, and this role of glycoproteins may be associated with the triggering of long-term memory formation by noradrenaline.
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PMID:2-deoxygalactose interferes with an intermediate processing stage of memory. 806 75

The transition from short- to long-term memory requires lasting modulations of synaptic connectivity. In a variety of species and learning tasks, enhanced synthesis of glycoprotein cell-adhesion molecules (CAMs), such as neural CAM (NCAM) and Ll, 5-8 h post-training is a necessary step in this process. If the training event is weak, this phase of glycoprotein synthesis does not occur and memory is not retained. Antibodies or fragments that bind to the extracellular domains of NCAM or Ll at this time produce amnesia for the task. Centrally administered corticosterone enhances retention of weak learning, and steroid-receptor antagonists are amnestic. The effects of corticosterone are mediated through synthesis of 'second-wave' glycoproteins. As 'nootropic' drugs such as piracetam only enhance long-term retention and are ineffective in adrenalectomized animals, the interaction between glucocorticoids and glycoproteins might provide a site for pharmacological intervention in alleviating the losses of memory that occur in neurodegenerative disorders.
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PMID:Cell-adhesion molecules, glucocorticoids and long-term-memory formation. 859 60

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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PMID: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. 1046 63


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