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)

The effects of BZ drugs result from interaction at the GABAA receptor within the CNS, producing anxiolysis, hypnosis, and amnesia in a dose-dependent fashion. These sedative effects are best titrated to reproducible clinical endpoints, using scoring systems such as the Ramsay scale. All BZs exhibit similar pharmacologic effects, but the important differences in pharmacokinetics and pharmacodynamics should be recognized to use these drugs safely and effectively within the ICU. Diazepam is the classic anxiolytic, amnestic, and sedative agent, but the presence of long-acting active metabolites that depend on the kidneys for elimination limits its use in many ICU patients. Lorazepam is the most potent BZ used in the ICU; it has stable pharmacokinetics and relatively low cost. This drug is best reserved for situations in which rapid onset is not essential and long-term sedation is anticipated. Midazolam has the shortest t1/2 of the commonly used BZs, generates few active metabolites, and is water soluble at physiologic pH. Thus, it is well suited for continuous infusion in the ICU, and the recent introduction of generic formulations of midazolam has decreased the drug-acquisition cost for many hospitals. Optimal sedation for ICU patients often requires BZ and concomitant therapy with drugs such as haloperidol, dexmedetomidine, opioids, and so forth, to reduce untoward side effects and, perhaps, overall drug costs. Flumazenil, a specific BZ antagonist, can be used for diagnostic or therapeutic reversal of BZ agonists when appropriate. Most experienced intensivists recommend an individualized approach to sedation and titration of anxiolysis to maximize efficacy, minimize side effects, and optimize cost effectiveness in the ICU. New CNS monitors of the EEG, such as the BIS or entropy EEG monitors, may refine titration algorithms further in the near future.
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PMID:Benzodiazepines in the intensive care unit. 1176 64

This report describes a case of amnesia during a cold-water experiment. The volunteer was exposed three times in 1 day (120 min duration each time) to 20 degrees C water. During the third immersion, from min 95 to min 115, the subject experienced transient global amnesia for 20 min. The rectal temperature during this time was 35.6 degrees C. This single case demonstrates that memory loss in a young individual apparently can occur after cold-water exposure and at core temperatures above 35 degrees C.
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PMID:Amnesia during cold water immersion: a case report. 1199 Jan 87

DM235 (sunifiram), a new compound structurally related to piracetam, prevented the amnesia induced by scopolamine (1.5 mg kg(-1) i.p.), after intraperitoneal (0.001-0.1 mg kg(-1)) or oral (0.01-0.1 mg kg(-1)) administration, as shown by a passive avoidance test in mice. The antiamnesic effect of DM235 was comparable to that of well-known nootropic drugs such as piracetam (30-100 mg kg(-1) i.p.), aniracetam (100 mg kg(-1) p.o.) or rolipram (30 mg kg(-1) p.o.). DM235 also prevented mecamylamine (20 mg kg(-1) i.p.)-, baclofen (2 mg kg(-1) i.p.)- and clonidine (0.125 mg kg(-1) i.p.)-induced amnesia in the same test. In the Morris water maze test with rats, scopolamine (0.8 mg kg(-1) i.p.) inhibited the reduction of escape latency in both acquisition and retention/retraining tests. DM235 (0.1 mg kg(-1) i.p.), 20 min before each daily acquisition training, prevented the scopolamine-induced memory impairment. DM235 (1 mg kg(-1) i.p.) also reduced the duration of pentobarbitone-induced hypnosis in mice without modifying the induction time of hypnosis. At the highest effective doses, the investigated compound neither impaired motor coordination (rota-rod test), nor modified spontaneous motility and inspection activity (Animex and hole board tests). These results indicate that DM235, a compound structurally related to piracetam, is a novel nootropic endowed with the capability to prevent cognitive deficits at very low doses. Indeed, its potency is about 1,000 times higher than that of the most active piracetam-like compounds.
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PMID:DM235 (sunifiram): a novel nootropic with potential as a cognitive enhancer. 1207 Jul 54

We previously reported that a total methanolic extract of the underground part of Angelica gigas Nakai (Umbelliferae) (here-in-after abbreviated AG) significantly inhibited acetylcholinesterase (AChE) activity. We characterized 12 coumarin derivatives including both decursin and decursinol from extracts of AG. In this study, we evaluated the anti-amnestic activity of decursin, a major coumarin constituent isolated from AG, in vivo using ICR mice with amnesia induced by scopolamine (1 mg/kg body weight, s.c.). Decursin, when administered to mice at 1 and 5 mg/kg body weight i.p., significantly ameliorated scopolamine-induced amnesia as measured in both the passive avoidance test and the Morris water maze test. Moreover, decursin significantly inhibited AChE activity by 34% in the hippocampus of treated mice. These results indicate that decursin may exert anti-amnestic activity in vivo through inhibition of AChE activity in the hippocampus.
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PMID:Decursin from Angelica gigas mitigates amnesia induced by scopolamine in mice. 1248 74

The present study determined whether peripheral injections of the 5HT(1A) agonist (8-OH-DPAT), scopolamine infusions into the frontal cortex, or a combination of both drug treatments would produce impairments in rats trained on passive avoidance. Using a 2x2 design, rats were infused with either bacteriostatic water or 30 microg/1 microl of scopolamine HCl into the frontal cortex 30 min before being trained on passive avoidance. This was followed by injections (ip) of either 0.1% ascorbic acid/bacteriostatic water or 30 microg/kg of 8-OH-DPAT 15 min later. All subjects were tested for retention 72h later. At test, the initial latency to enter into the black shocked compartment and the total time spent in the white safe compartment (TTW) were recorded. Analysis of the latency data indicated that scopolamine and 8-OH-DPAT, when administered singly or in combination, produced amnesia for the task. Assessment of TTW scores, however, revealed that of the three drug-treated groups, only animals treated with 8-OH-DPAT alone tended to avoid the previously shocked black compartment and spend more time in the white safe compartment. These data indicate that either stimulating 5-HT(1A) or blocking frontal cortical muscarinic receptors at training impairs passive avoidance performance and that the deficit following the latter treatment is somewhat more extensive. Implications for the role frontal cortical muscarinic and 5HT(1A) receptors play in learning and memory are discussed.
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PMID:Peripheral 8-OH-DPAT and scopolamine infused into the frontal cortex produce passive avoidance retention impairments in rats. 1259 Dec 22

(1) Dimemorfan, an antitussive for more than 25 years, has previously been reported to be a relative high-affinity ligand at sigma-1 (sigma(1)) receptor with the K(i) value of 151 nM. (2) To test whether dimemorfan has anti-amnesic effects similar to a sigma(1) receptor agonist, this study examined its effects on scopolamine- and beta-amyloid peptide-(25-35)-induced amnesia in mice. (3) Dimemorfan (10-40 mg kg(-1), i.p.) administered 30 min before the training trial, immediately after the training trial, or 30 min before the retention test significantly improved scopolamine (1 mg kg(-1), i.p.)- or beta-amyloid peptide-(25-35) (3 nmol mouse(-1), i.c.v.)-induced amnesia in a step-through passive avoidance test. Dimemorfan (5-40 mg kg(-1), i.p.) pretreatment also attenuated scopolamine (8 mg kg(-1), i.p.)-induced amnesia in a water-maze test. And, these anti-amnesic effects of dimemorfan, like the putative sigma(1) receptor agonist (+)-N-allylnormetazocine ((+)-SKF-10047), were antagonized by a sigma receptor antagonist haloperidol (0.25 mg kg(-1), i.p.). (4) These results indicated that dimemorfan has anti-amnesic effects and acts like a sigma(1) receptor agonist.
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PMID:Anti-amnesic effect of dimemorfan in mice. 1264 96

We previously reported that phenylpropanoids isolated from the roots of Scrophularia buergeriana Miquel (Scrophulariaceae) protected cultured cortical neurons against glutamate-induced neurotoxicity [Kim and Kim, Phytochemistry, 54 (2000) 503-509; Kim et al., Br. J. Pharmacol. 135 (2002) 1281-1291]. In the present study, we examined the anti-amnestic activities of phenylpropanoids in mice with amnesia induced in vivo by scopolamine. Among the phenylpropanoids tested through passive avoidance tasks, buergeriside A1, buergeriside C1, E-p-methoxycinnamic acid (E-p-MCA) and E-isoferulic acid significantly improved the deficit of memory induced by scopolamine. This suggested that the alpha,beta-unsaturated carboxyl moiety and the para-methoxy group in phenylpropanoids (E-p-MCA) might be a crucial component in their cognition-enhancing activity. Indeed, E-p-MCA (0.01-2 mg/kg body weight, i.p.), given in pre- or post-treatment paradigms, significantly ameliorated scopolamine-induced amnesia as determined by passive avoidance tasks and prevented or aided in the recovery of memory to a level that was about 60% of control. In addition, E-p-MCA (0.1-1.0 mg/kg body weight, i.p.) significantly improved impairments of spatial learning and memory induced by scopolamine; the compound reduced deficits in both long- and short-term memories as measured by the Morris water maze test. We suggest, therefore, that E-p-MCA may ultimately hold significant therapeutic value in alleviating certain memory impairments observed in dementia.
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PMID:Anti-amnestic activity of E-p-methoxycinnamic acid from Scrophularia buergeriana. 1288 Sep 15

Cannabinoids, the active components of marijuana, affect memory and hippocampal neurotransmission. It has been claimed that nabilone, a synthetic cannabinoid endowed with antiemetic properties, has a peculiar profile of actions. We studied the effects of the drug on spatial learning and in vitro hippocampal CA1 electrophysiology in the rat. Nabilone (0.1, 0.5, and 1.0 mg/kg ip) does not impair place learning in a water maze task, whereas Delta(8)-tetrahydrocannabinol (Delta(8)-THC) disrupts this function. At concentrations ranging from 1 nM to 10 microM nabilone does not influence basal glutamatergic neurotransmission, which is decreased by Delta(8)-THC. Although cannabinoids have been consistently reported to affect synaptic plasticity, nabilone 1 microM does not change paired-pulse facilitation, long-term potentiation and the magnitude of long-term depression. However, the time course of the latter phenomenon is significantly changed by the drug, the depression being lower than in control experiments from 7 to 35 min postinduction. Altogether, our data indicate that there might be differences in the effects of agonists for central cannabinoid receptors, which could help to understand the pharmacology of this class of molecules. The results also suggest that amnesia induced by cannabinoids be possibly related to their effects on hippocampal neurotransmission. The study supports the use of nabilone in conditions the course of which is complicated by cognitive impairment.
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PMID:Effects of the synthetic cannabinoid nabilone on spatial learning and hippocampal neurotransmission. 1289 76

It is suggested to reproduce a retrograde amnesia in mice by means of a complex extremal action: emaciating swim in cold water with simultaneous wheel rotation. It was found that nootropes such as pyracetam, mexidol, semax, nooglutil, acephen, and noopept fully or completely prevent from the amnesia development.
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PMID:[A method for reproducing amnesia in mice by the complex extremal exposure]. 1292 40

The highly potent and selective 5-HT(6) receptor antagonist SB-271046 [5-chloro-N-(4-methoxy-3-piperazin-1-yl-phenyl)-3-methyl-2-benzothiophenesulfonamide] has previously been demonstrated to improve retention significantly in a spatial water maze paradigm in adult rats. However, SB-271046 did not have any effect on task acquisition. As these apparently contradictory findings may be reconciled by a prime influence of SB-271046 on memory consolidation, the ability of this compound to reverse the discrete temporal action of a cholinergic antagonist in the 6-h period following passive avoidance training was investigated. SB-271046, given orally, by gavage, 30 min prior to training Wistar rats in a step-through, light-dark passive avoidance task, was found to reverse significantly the amnesia produced by administering scopolamine (0.8 mg/kg, intraperitoneal) in the 6-h post-training period. The effect was dose-dependent over a range of 3-20 mg/kg. Further, we investigated the cognition-enhancing effects of chronic SB-271046 administration (10 or 20 mg/kg/day; 40 days) on the acquisition and consolidation of a water maze spatial learning task in a population of 20-month-old Wistar rats with age-related learning deficits. Drug treatment progressively and significantly decreased platform swim angle and escape latencies over the five sequential trials on four consecutive daily sessions compared to vehicle-treated controls. SB-271046 also improved task recall as measured by significant increases in the searching of the target quadrant on post-training days 1 and 3, when the animals would have been substantially drug-free. This significant improvement of task recall suggests SB-271046, in addition to inducing symptomatic cognition-enhancing actions, also attenuates age-related decline in neural function.
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PMID:The 5-HT(6) receptor antagonist SB-271046 reverses scopolamine-disrupted consolidation of a passive avoidance task and ameliorates spatial task deficits in aged rats. 1457 Dec 56


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