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Query: UMLS:C0002622 (amnesia)
 5,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
Neurobiol Learn Mem 1997 Jan
PMID:Antibody to day-old chick brain glycoprotein produces amnesia in adult rats. 901 96

The cellular expression of S-100 beta protein is upregulated in Alzheimer's disease and in Down's syndrome, and this protein has been implicated in memory-related processes in laboratory animals. However, the possibility that the alpha subunit of S-100 is also involved in memory has not yet been examined. In the present study, day-old black Australorp white Leghorn cockerel chicks (Gallus domesticus) received injections of monoclonal antisera to S-100 alpha (1:50) or S-100 beta (1:500) into each hemisphere immediately after training on a one-trial passive avoidance task. The chicks displayed significantly lower retention levels than control birds that had been injected with antisera to carbonic anhydrase, or with saline (p < .01). S-100 alpha antisera had an amnestic effect when injected between 0 and 20 min after training, with memory deficits occurring from 30 min post-learning, at the point of transition between the A and the B phases of the Gibbs-Ng intermediate memory stage. By contrast, the S-100 beta antisera needed to be injected either 5 min before or immediately after training and produced amnesia 10 min earlier, at the start of the A phase of the intermediate memory stage. We conclude that the two subunits of the S-100 protein are required at different points in the sequence of events leading to the consolidation of passive avoidance memory.
Neurobiol Learn Mem 1997 May
PMID:Chicks injected with antisera to either S-100 alpha or S-100 beta protein develop amnesia for a passive avoidance task. 915 58

Retrograde amnesia was induced in rats trained in step-down inhibitory avoidance by four different treatments: an ip injection of beta-endorphin (1.0 microgram kg), an electroconvulsive shock (ECS), an intrahippocampal infusion of the calcium/calmodulin protein kinase II inhibitor, KN62 (0.08 microgram/side), given 0 h after training, or an intrahippocampal infusion of the protein kinase A inhibitor, KT5720 (0.5 microgram/side), given 3 h after training. Pretest ip injections of ACTH (0.2 microgram/kg) or vasopressin (10.0 micrograms/kg), but not saline, reversed the amnesia caused by beta-endorphin and ECS but not that caused by the enzyme inhibitors. This suggests that the amnesia produced by intrahippocampal KN62 and KT5720 administration is stronger than that caused by ECS and beta-endorphin, possibly because the former interfere directly with specific steps of the core biochemical chain of events that underlies memory consolidation.
Neurobiol Learn Mem 1997 Sep
PMID:Systemic administration of ACTH or vasopressin reverses the amnestic effect of posttraining beta-endorphin or electroconvulsive shock but not that of intrahippocampal infusion of protein kinase inhibitors. 932 61

Although protein synthesis inhibition has been shown to affect long-term memory in a wide variety of animal species, cases have been reported in which protein synthesis inhibition failed to affect memory consolidation [S. Wittstock, R. Menzel, Color learning and memory in honey bees are not affected by protein synthesis inhibition, Behav. Neural Biol., 62 (1994) 224-229.]. Most findings argue that the critical time for protein synthesis is during or immediately after training. However, other reports show a second time window, hours after training, where protein synthesis inhibition can cause amnesia [F.M. Freeman, S.P.R. Rose, A.B. Scholey, Two time windows of anisomycin-induced amnesia for passive avoidance training in the day-old chick, Neurobiol. Learn. Mem., 63 (1995) 291-295.][G. Grecksch, H. Matthies, Two sensitive periods for the amnesic effect of anisomycin, Pharmacol. Biochem. Behav., 12 (1980) 663-665.]. In this study, we addressed two questions: (1) Is protein synthesis essential for spatial memory? and (2) At what injection time window(s) will protein synthesis inhibition cause spatial memory amnesia? We report that bilateral intraventricular microinjection of anisomycin (Ani) impairs consolidation of long-term memory, in the hippocampal-dependent Morris water maze spatial memory task. Memory was impaired in a dose-dependent manner without affecting short-term memory. Spatial memory was affected only if Ani was injected 20 min before performing the task and not in any other time window before or after the behavioral test. The inhibition did not affect pre-existing memories or the capability to memorize once the effect of the inhibition diminished.
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PMID:Lateral ventricle injection of the protein synthesis inhibitor anisomycin impairs long-term memory in a spatial memory task. 960 54

The antibiotic chloramphenicol, an inhibitor of mitochondrial protein synthesis, was used to investigate the time-related changes in protein synthesis following passive avoidance training in the day-old chick (white leghorn-black Australorp). Retention of memory for this simple learning task is known to be prevented by an inhibitor of cytosolic protein synthesis, anisomycin, in a biphasic manner, with the first phase of sensitivity occurring up to 90 min post-training and the second phase between 4 and 5 h post-training (Freeman, Rose, & Scholey, 1995). Birds received bilateral intracranial injections of chloramphenicol (10 microl/hemisphere of a 7.4 mM solution) at various times relative to training and were tested 24 h later. This report shows that at the second phase of anisomycin susceptibility there was a chloramphenicol-sensitive period (5 h post-training) which had an onset time less than 1 h after injection. The effect of chloramphenicol appears not to be due to the mitochondria being energetically compromised since intracranial injections of an uncoupler of mitochondrial oxidative phosphorylation, 2,4-dinitrophenol (0.1 mM), did not disrupt memory formation when injected 5 h after training, even though it did cause amnesia when injected at the earlier time point of 20 min post-training. These results are discussed in the context of what is already known about memory formation in the day-old chick.
Neurobiol Learn Mem 1999 Jan
PMID:Chloramphenicol-induced amnesia for passive avoidance training in the day-old chick. 988 74

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.
Learn Mem
PMID:Sequence-specific impairment of memory formation by NCAM antisense oligonucleotides. 1032 37

Metabotropic glutamate receptors (mGluRs) have been implicated in long-term potentiation and in learning and memory formation. In this study, we tested the effects of group I mGluR inhibition on synaptic plasticity and learning of rats at different levels of organization (1) in the hippocampal slice preparation; (2) in freely moving animals implanted with chronic hippocampal electrodes; and (3) in different spatial learning paradigms. To allow a direct comparison of the effects obtained the same doses were used in all paradigms. Bath-application of the selective group I mGluR antagonist (S)4-carboxyphenylglycine (4-CPG) impaired a decremental long-term potentiation (LTP) induced by a weak tetanization paradigm, but failed to affect a robust LTP generated by strong tetanization. In contrast, 4-CPG impaired a robust LTP in freely moving animals if applied 30 min before tetanization. The same dose of 4-CPG only impeded spatial learning mildly in the eight-arm radial maze and had no effect on a simple configuration of the Y-maze spatial alternation task. In the more difficult configuration of this task, however, 4-CPG caused complete amnesia. The lack of state-dependent 4-CPG actions and the absence of any 4-CPG effects in the open-field test classify the obtained retention deficit as a selective impairment of memory storage. Our results indicate a specific role of group I mGluRs in certain types of synaptic plasticity and of spatial learning.
Learn Mem
PMID:A specific role for group I mGluRs in hippocampal LTP and hippocampus-dependent spatial learning. 1032 39

Three experiments explored the rate at which amnesic participants' free recall, cued recall, and recognition of prose declined over short filled delays. In Experiment 1, after performance had been matched to that of controls at 15s, amnesics showed accelerated forgetting over delays of up to 10 min in a free-recall condition, whereas recognition performance declined normally over delays of up to 1 hr. This pattern of results was replicated in Experiment 2, which showed that amnesic rate of forgetting on a test of cued recall was influenced by level of cuing. Experiment 3 showed that excessive sensitivity to interference was unlikely to be the cause of the amnesic patients' accelerated forgetting rate, which is instead explained in terms of storage deficit accounts of amnesia.
J Exp Psychol Learn Mem Cogn 1999 Jul
PMID:Rate of forgetting in amnesia: I. Recall and recognition of prose. 1043 2

We have used a combined genetic and pharmacological approach to define the time course of the requirement for protein kinase A (PKA) and protein synthesis in long-term memory for contextual fear conditioning in mice. The time course of amnesia in transgenic mice that express R(AB) and have genetically reduced PKA activity in the hippocampus parallels that observed both in mice treated with inhibitors of PKA and mice treated with inhibitors of protein synthesis. This PKA- and protein synthesis-dependent memory develops between 1 hr and 3 hr after training. By injecting the protein synthesis inhibitor anisomycin or the PKA inhibitor Rp-cAMPs at various times after training, we find that depending on the nature of training, contextual memory has either one or two brief consolidation periods requiring synthesis of new proteins, and each of these also requires PKA. Weak training shows two time periods of sensitivity to inhibitors of protein synthesis and PKA, whereas stronger training exhibits only one. These studies underscore the parallel dependence of long-term contextual memory on protein synthesis and PKA and suggest that different training protocols may recruit a common signaling pathway in distinct ways.
Learn Mem
PMID:Different training procedures recruit either one or two critical periods for contextual memory consolidation, each of which requires protein synthesis and PKA. 1045 61

Emotional arousal has been demonstrated to enhance declarative memory (conscious recollection) in humans in both naturalistic and experimental studies. Here, we examined this effect in amnesia. Amnesic patients and controls viewed a slide presentation while listening to an accompanying emotionally arousing story. In both groups, recognition memory was enhanced for the emotionally arousing story elements. The magnitude of the enhancement was proportional for both amnesic patients and controls. Emotional reactions to the story were also equivalent. The results suggest that the enhancement of declarative memory associated with emotional arousal is intact in amnesia. Together with findings from patients with bilateral amygdala lesions, the results indicate that the amygdala is responsible for the enhancement effect.
Learn Mem
PMID:Intact enhancement of declarative memory for emotional material in amnesia. 1045 71


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