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

The ventral subiculum (vSUB), a hippocampal efferent target implicated in learning and stress coping, receives cholinergic input and sends glutamatergic output to the bed nucleus of the stria terminalis (BNST). This study examined the roles of vSUB muscarinic activation and its interaction with BNST N-methyl-D-aspartate and noradrenergic receptors in formation of aversive memory. Male Wistar rats with cannulae implanted into the vSUB or BNST were trained on a step-through inhibitory avoidance task. Shortly after training, they received cholinergic drugs infused into the vSUB and/or glutamatergic or noradrenergic drugs infused into the BNST. Results of the 1-day retention tests showed that intra-vSUB infusion of oxotremorine (0.01 microg) or scopolamine (0.3 or 3.0 microg) enhanced or impaired retention, respectively. Both effects were dose- and time-dependent, and 0.001 microg oxotremorine attenuated the amnesia induced by 3.0 microg scopolamine. The oxotremorine-induced memory enhancement was blocked by intra-BNST infusion of DL-2-amino-5-phosphonovaleric acid or propranolol at a dose not affecting retention; the amnesia induced by scopolamine was blunted by intra-BNST infusion of glutamate or norepinephrine at a dose with a negligible effect on retention. These data suggest that in an inhibitory avoidance task muscarinic activation of the vSUB modulated memory formation by interacting with the BNST glutamatergic and noradrenergic functions.
Neurobiol Learn Mem 2009 Mar
PMID:Posttraining infusion of cholinergic drugs into the ventral subiculum modulated memory in an inhibitory avoidance task: interaction with the bed nucleus of the stria terminalis. 1904 26

Defendants who are accused of serious crimes sometimes feign amnesia to evade criminal responsibility. Previous research has suggested that feigning amnesia might impair subsequent recall. In two experiments, participants read and heard a story about a central character, described as "you," who was responsible for the death of either a puppy (Experiment 1) or a friend (Experiment 2). On free and cued recall tests immediately after the story, participants who had feigned amnesia recalled less than did participants who had recalled accurately. One week later, when all participants recalled accurately, participants who had previously feigned amnesia still performed worse than did participants who had recalled accurately both times. However, the participants who had formerly feigned amnesia did not perform worse than did a control group who had received only the delayed recall tests. Our results suggest that a "feigned amnesia effect" may reflect nothing more than differential practice at recall. Feigning amnesia for a crime need not impair memory for that crime when a person later seeks to remember accurately.
Mem Cognit 2009 Jan
PMID:Does feigning amnesia impair subsequent recall? 1910 78

The IRAP ligands Angiotensin IV (Ang IV) and LVV-haemorphin 7 (LVV-H7) enhance performance in a range of memory paradigms in normal rats and ameliorate memory deficits in rat models for amnesia. The mechanism by which these peptides facilitate memory remains to be elucidated. In recent in vitro experiments, we demonstrated that Ang IV and LVV-H7 potentiate activity-evoked glucose uptake into hippocampal neurons. This raises the possibility that IRAP ligands may facilitate memory in hippocampus-dependent tasks through enhancement of hippocampal glucose uptake. Acute intracerebroventricular (i.c.v.) administration of 1nmol Ang IV or 0.1nmol LVV-H7 in 3 months-old Sprague-Dawley rats enhanced spatial working memory in the plus maze spontaneous alternation task. Extracellular hippocampal glucose levels were monitored before, during and after behavioral testing using in vivo microdialysis. Extracellular hippocampal glucose levels decreased significantly to about 70% of baseline when the animals explored the plus maze, but remained constant when the animals were placed into a novel control chamber. Ang IV and LVV-H7 did not significantly alter hippocampal glucose levels compared to control animals in the plus maze or control chamber. Both peptides had no effect on hippocampal blood flow as determined by laser Doppler flowmetry, excluding that either peptide increased the hippocampal supply of glucose. We demonstrated for the first time that Ang IV and LVV-H7 enhance spatial working memory in the plus maze spontaneous alternation task but no in vivo evidence was found for enhanced hippocampal glucose uptake or blood flow.
Neurobiol Learn Mem 2009 Jul
PMID:Angiotensin IV and LVV-haemorphin 7 enhance spatial working memory in rats: effects on hippocampal glucose levels and blood flow. 1923 1

To this day, it remains unresolved whether experimental amnesia reflects failed memory storage or the inability to retrieve otherwise intact memory. Methodological as well as conceptual reasons prevented deciding between these two alternatives: The absence of recovery from amnesia is typically taken as supporting storage impairment interpretations; however, this absence of recovery does not positively demonstrate nonexistence of memory, allowing for alternative interpretations of amnesia as impairment of memory retrieval. To address this shortcoming, we present a novel approach to study the nature of amnesia that makes positive, i.e., falsifiable, predictions for the absence of memory. Applying this paradigm, we demonstrate here that infusing anisomycin into the dorsal hippocampus induces amnesia by impairing memory storage, not retrieval.
Learn Mem 2009 Apr
PMID:Storage or retrieval deficit: the yin and yang of amnesia. 1985 Jun 66

Dextro-amphetamine enhances memory and other cognitive functions in animals and humans. The use of d-amphetamine as a memory enhancer, however, is limited by a robust stimulatory side-effect profile caused by release of dopamine. The levo enantiomer of amphetamine has been shown to be considerably less effective as a dopamine releaser and less potent in producing the stimulatory effects characteristic of d-amphetamine. In order to determine whether l-amphetamine and the structurally related compound, l-methamphetamine, retain cognitive-enhancing effects despite their lack of stimulatory activity, we administered the compounds to rats prior to activity monitoring experiments, and in different animals, immediately after training on inhibitory avoidance and object recognition tasks. Results demonstrated that l-amphetamine and l-methamphetamine did not increase locomotion and stereotypies beyond control levels, but did produce significant memory enhancement. In addition, l-amphetamine and l-methamphetamine alleviated scopolamine-induced amnesia in the inhibitory avoidance task. In all cases, these compounds produced an effect comparable to that of d-amphetamine, but required only one quarter of the d-amphetamine dose to produce the same effect size. We also found that l-amphetamine modulates learning-induced changes in hippocampal Arc/Arg3.1 protein synthesis that correlate with memory consolidation. These results suggest that l-amphetamine and l-methamphetamine are potent memory enhancers in rats and may ultimately be useful for treating memory disorders in humans.
Neurobiol Learn Mem 2009 Jul
PMID:The levo enantiomer of amphetamine increases memory consolidation and gene expression in the hippocampus without producing locomotor stimulation. 1936 65

Intra-amygdala injections of anisomycin produce large increases in the release of norepinephrine (NE), dopamine (DA), and serotonin in the amygdala. Pretreatment with intra-amygdala injections of the beta-adrenergic receptor antagonist propranolol attenuates anisomycin-induced amnesia without reversing the inhibition of protein synthesis, and injections of NE alone produce amnesia. These findings suggest that abnormal neurotransmitter responses may be the basis for amnesia produced by inhibition of protein synthesis. The present experiment extends these findings to the hippocampus and adds acetylcholine (ACh) to the list of neurotransmitters affected by anisomycin. Using in vivo microdialysis at the site of injection, release of NE, DA, and ACh was measured before and after injections of anisomycin into the hippocampus. Anisomycin impaired inhibitory avoidance memory when rats were tested 48 h after training and also produced substantial increases in local release of NE, DA, and ACh. In an additional experiment, pretreatment with intrahippocampal injections of propranolol prior to anisomycin and training significantly attenuated anisomycin-induced amnesia. The disruption of neurotransmitter release patterns at the site of injection appears to contribute significantly to the mechanisms underlying amnesia produced by protein synthesis inhibitors, calling into question the dominant interpretation that the amnesia reflects loss of training-initiated protein synthesis necessary for memory formation. Instead, the findings suggest that proteins needed for memory formation are available prior to an experience, and that post-translational modifications of these proteins may be sufficient to enable the formation of new memories.
Learn Mem 2009 May
PMID:Intrahippocampal infusions of anisomycin produce amnesia: contribution of increased release of norepinephrine, dopamine, and acetylcholine. 1940 93

In the present study, the effects of intra-dorsal hippocampus (intra-CA1) injection of cannabinoid receptor agents on memory formation have been investigated in 3-days apomorphine-treated rats. Step-through inhibitory avoidance task of memory has been used to examine retrieval of memory formation, 24h after training. Apomorphine was injected subcutaneously (S.C.), once daily for 3-days followed by 5 days free of the apomorphine before training. Bilateral post-training intra-CA1 infusions of the non selective CB1-CB2 receptor agonist, WIN55,212-2 (0.1, 0.25 and 0.5 microg/rat), dose-dependently shortened the step-through latency, suggesting amnesia by the drug, whereas bilateral post-training intra-CA1 micro-injections of the selective CB1 receptor antagonist, AM251 (25, 50 and 100 ng/rat), did not affect memory formation. Intra-CA1 infusions of AM251 and WIN55,212-2, two min apart, modify the WIN55,212-2-induced reduction of step-through latency. Furthermore, the deleterious effect of WIN55,212-2 (0.25 microg/rat) was completely abolished in rats previously given apomorphine (0.5 and 1 mg/kg/day, S.C.) for 3 days. This prevention of WIN55,212-2-induced amnestic-like effect was counteracted by the dopamine D2 receptor antagonist, sulpiride (0.25, 0.5 and 1 mg/kg/day x 3-days, S.C.), administered 30 min before each injection of apomorphine (0.5 mg/kg/day x 3-days, S.C.). The D1 receptor antagonist, SCH 23390 (0.01, 0.02, 0.07 and 0.1 mg/kg/day x 3-days, S.C.), was ineffective in this respect. The results suggest that subchronic apomorphine treatment may induce dopamine D2 receptor sensitization, which in turn prevented amnesia induced by WIN55,212-2.
Neurobiol Learn Mem 2009 Oct
PMID:Effects of cannabinoids infused into the dorsal hippocampus upon memory formation in 3-days apomorphine-treated rats. 1945 Jun 98

Accuracy in identifying a perceptually degraded word (e.g., stake) can be either enhanced by recent exposure to the same stimulus or reduced by recent exposure to a similar stimulus (e.g., stare). In the present study, we explored the mechanisms underlying these benefits and costs by examining the performance of amnesic and control groups in a forced choice perceptual identification (FCPI) task in which briefly flashed words (that were identical to studied words, similar to studied words, or new) had to be identified, and two response choices were provided that differed from each other by one letter. Control participants showed a performance benefit and cost in FCPI with both high- and low-frequency words. Amnesic participants showed a benefit (but no cost) with high-frequency words and a benefit and a cost with low-frequency words. The benefit/cost pattern with low-frequency words in amnesia was obtained even when the to-be-identified stimulus in the FCPI task was eliminated (Experiment 2), suggesting that this effect was driven by processes operating at the level of the response choices. Our findings suggest that implicit memory effects in FCPI reflect the operation of multiple mechanisms, the relative contributions of which may vary with the frequency of the test stimuli. The results also highlight the need for caution in interpreting results from normal participants in the FCPI task, since those findings may reflect a contribution of explicit memory processes.
Mem Cognit 2009 Jul
PMID:Performance benefits and costs in forced choice perceptual identification in amnesia: Effects of prior exposure and word frequency. 1948 57

Growing evidence indicates that antagonists of the 5-hydroxytryptamine (serotonin) receptor(6) (5-HT(6)) improve memory and reverse amnesia although the mechanisms involved are poorly understood. Hence, in this paper RT-PCR was used to evaluate changes in mRNA expression of 5-HT(6) receptor in trained and untrained rats treated with the 5-HT(6) receptor antagonist SB-399885 and amnesic drugs scopolamine or dizocilpine. Changes in mRNA expression of 5-HT(6) receptor were investigated at different times in prefrontal cortex, hippocampus and striatum. Data indicated that memory in the Pavlovian/instrumental autoshaping task was a progressive process associated to reduced mRNA expression of 5-HT(6) receptor in the three structures examined. SB-399885 improved long-term memory at 48h, while the muscarinic receptor antagonist scopolamine or the non-competitive NMDA receptor antagonist dizocilpine impaired it at 24h. Autoshaping training and treatment with SB-399885 increased 5-HT(6) receptor mRNA expression in (maximum increase) prefrontal cortex and striatum, 24 or 48h. The scopolamine-induced amnesia suppressed 5-HT(6) receptor mRNA expression while the dizocilpine-induced amnesia did not modify 5-HT(6) receptor mRNA expression. SB-399885 and scopolamine or dizocilpine were able to reestablish memory and 5-HT(6) receptor mRNA expression. These data confirmed previous memory evidence and of more interest is the observation that training, SB-399885 and amnesic drugs modulated 5-HT(6) receptor mRNA expression in prefrontal cortex, hippocampus and striatum. Further investigation in different memory tasks, times and amnesia models together with more complex control groups might provide further clues.
Neurobiol Learn Mem 2010 Jan
PMID:Time-course of 5-HT(6) receptor mRNA expression during memory consolidation and amnesia. 1973 50

A considerable literature has shown deficits in memory resulting from the administration of protein synthesis inhibitors; however, most of the past literature in this field has focused on acquisition of new memory using aversively-motivated tasks. The effect of protein synthesis inhibition on appetitive learning and memory as well as extinction is less clear. The present study employed an appetitive odor discrimination paradigm to examine the effects of acute cycloheximide administration (1mg/kg) on reconsolidation and extinction. Male, Long-Evans adult rats were trained to discriminate between two odors (i.e., cocoa and cinnamon) and then received extinction trials following an intraperitoneal injection of cycloheximide or vehicle. Twenty-four hours later, rats were tested via one non-reinforced test trial. Results showed amnesia for extinction as well as original training (i.e., correct odor choice) in cycloheximide-injected rats in this appetitive task, while vehicle-injected controls showed good memory for extinction. These data add to a growing literature showing the importance of protein synthesis inhibition for extinction and reconsolidation in appetitive learning and memory.
Neurobiol Learn Mem 2010 Jan
PMID:Cycloheximide produces amnesia for extinction and reconsolidation in an appetitive odor discrimination task in rats. 1976 62


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