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 N-methyl-D-aspartate NMDA receptor antagonists on scopolamine-induced amnesia and on delay-interposed short-term memory performance were investigated using an 8-arm radial maze in rats. Scopolamine, a muscarinic antagonist, deteriorated the radial maze performance, while MK-801, an NMDA receptor channel blocker and CGS-19755, a competitive NMDA receptor antagonist, showed no obstruction to the spatial cognition in the non-delayed maze task. MK-801 (0.01-0.03 mg/kg, i.v.) and CGS-19755 (1-10 mg/kg, i.v.) significantly augmented scopolamine-induced deficit in the non-delayed maze task and impaired the short-term memory in the 5-min delay-interposed task. These results suggest that NMDA antagonists have a negative action on short-term memory and that the interaction between the NMDA and the central muscarinic system plays a role in modulating the cognitive function.
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PMID:NMDA antagonists potentiate scopolamine-induced amnesic effect. 906 90

The effects of rolipram, a cAMP-specific phosphodiesterase (phosphodiesterase 4) inhibitor, on experimentally-induced amnesia were examined using a 3-panel runway paradigm in rats and a passive avoidance task in mice. Scopolamine, cerebral ischemia induced by four-vessel occlusion and electric convulsive shock impaired working memory in the 3-panel runway task. Rolipram at 0.1 mg/kg reduced the increase in errors induced by scopolamine or cerebral ischemia. Rolipram at 0.32 mg/kg also reduced the increase in errors induced by electric convulsive shock. Dibutyryl cAMP also had similar effects in 3-panel runway experiments. In the passive avoidance task, rolipram reversed the impairments of the avoidance response induced by scopolamine, cycloheximide and electric convulsive shock at 10, 10 and 3 mg/kg, respectively. These results indicate that rolipram ameliorates impairments of learning and memory in rats and mice, and suggest that rolipram might ameliorate the impairments of learning and memory by elevating cAMP levels.
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PMID:Ameliorating effects of rolipram on experimentally induced impairments of learning and memory in rodents. 908 37

Gastrodin (GAS) and p-hydroxybenzyl alcohol (HBA) which is an aglycone of gastrodin, are active ingredients of Gastrodia elata Blume. In this study, we attempted to investigate the effects of acute administration of GAS and HBA on learning and memory processes such as acquisition, consolidation and retrieval, on the passive avoidance task in rats; piracetam was used as a positive control. Scopolamine, impairing learning acquisition, shortened the step-through latency in the retention test in rats. GAS and HBA did not prolong the step-through latency induced by scopolamine in the passive avoidance task, but piracetam could prolong the step-through latency induced by scopolamine. Cycloheximide, impairing memory consolidation, shortened the step-through latency in the retention test in rats. GAS at 50 mg/kg, HBA at 5 mg/kg and piracetam at 100 mg/kg could prolong the step-through latency induced by cycloheximide in the passive avoidance task. Apomorphine, impairing memory retrieval, shortened the step-through latency in the retention test in rats. GAS at 5 mg/kg, HBA at 1 mg/kg and piracetam at 300 mg/kg could prolong the step-through latency induced by apomorphine in the passive avoidance task. From the above results, we concluded that the facilitating effects of HBA on learning and memory are better than those of GAS. In conclusion, GAS and HBA can improve cycloheximide- and apomorphine-induced amnesia, but not scopolamine-induced acquisition impairment in rats. Thus, GAS and HBA can facilitate memory consolidation and retrieval, but not acquisition. The facilitating effects of GAS and HBA are different from those of piracetam.
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PMID:Gastrodin and p-hydroxybenzyl alcohol facilitate memory consolidation and retrieval, but not acquisition, on the passive avoidance task in rats. 914 53

Previous research has shown that glucose is an effective agent in facilitating memory performance and in attenuating scopolamine-induced amnesia. Although insulin has not been shown to facilitate unimpaired memory, a previous study has demonstrated that insulin can also attenuate scopolamine-degraded memory. The present study was designed to determine how different combinations of insulin, glucose and scopolamine affect memory. It involved nine rats whose memory was assessed through performance in a win-shift radial arm maze task under different drug treatments. A 2 x 2 x 2 (insulin x glucose x scopolamine) within-subjects design with a 5-h drug test interval was employed. Scopolamine disrupted memory performance, and both glucose and insulin counteracted this disruption. Combining the glucose and insulin treatments did not increase their ability to attenuate scopolamine deficits but slightly decreased this effect. Glucose tended to enhance memory, even in the absence of scopolamine, whereas insulin had no effect on memory in the absence of scopolamine. Blood glucose levels were measured and did not indicate changes caused by drug treatments. The memory effects may have been due to the acetylcholine-agonist actions of glucose and insulin, an interpretation consistent with previous research findings.
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PMID:Effect of combinations of insulin, glucose and scopolamine on radial arm maze performance. 926 93

For the purpose of rational modification of the TRH molecule, we were pursuing an approach that consists of two steps: (1) 'obligatory' replacement of histidine with glutamine in TRH and (2) the application of conformational constraints for putative bioactive conformation I stabilized by an intramolecular hydrogen bond between C-terminal carboxamide proton and alpha-carbonyl of histidyl (glutaminyl), and conformation II formed by an intramolecular hydrogen bond between alpha-carbonyl of pyroglutamyl and prolinamide proton. Significant antiamnesic potency was discovered in the passive avoidance test (ECS and Scopolamine induced amnesia) for conformation II mimic (8S,10aS)-8-carbamoyl-1,2,3,6,7,8,9,10a- octahydro-5H,10H-pyrrolo[1,2-a][1,4]diazocin-5,10-dione (2) at doses of 0.1 and 1.0 mg/kg. EEG analysis indicates a mild activating effect of compound 2 on EEG, which is similar to that of piracetam and differs from hard amphetamine activation. Conformation I mimic 3-(2-carbamoylethyl)-2,3,6,7,8,8a-hexahydro-1H,4H-pyrrolo[1,2-a] pyrazin-1,4-dione (1) exhibited an antidepressant effect at a dose of 1 mg/kg. The transition from two putative quasi-cyclic bioactive conformations of TRH and its obligatory similar analogue [Gln2]-TRH to their cyclic mimics led to differentiation of antiamnesic and antidepressant activity of TRH.
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PMID:TRH mimetics: differentiation of antiamnesic potency from antidepressant effect. 941 20

Our previous studies have demonstrated that FK960 (FR59960; N-(4-acetyl-1-piperazinyl)-p-fluorobenzamide monohydrate), a novel antidementia piperazine derivative, exerts beneficial effects on memory deficits in various animal models of amnesia in rats [M. Yamazaki, N. Matsuoka, N. Maeda, Y. Ohkubo, I. Yamaguchi, FK960 N-(4-acetyl-1-piperazinyl)-p-fluorobenzamide monohydrate ameliorates the memory deficits in rats through a novel mechanism of action, J. Pharmacol. Exp. Ther., 279 (1996) 1157-1173.] and in rhesus monkeys [N. Matsuoka, T.G. Aigner, FK960 [N-(4-acetyl-1-piperazinyl)-p-fluorobenzamide monohydrate], a novel potential antidementia drug, improves visual recognition memory in rhesus monkeys: comparison with physostigmine, J. Pharmacol. Exp. Ther., 280 (1997) 1201-1209]. To clarify the synaptic mechanisms of its antiamnesic action, FK960 was investigated for its effects on the development of long-term potentiation (LTP) in guinea-pig hippocampal slices. The magnitude of LTP of population spike recorded in CA3 pyramidal neurons was significantly augmented by perfusing FK960 (10-9-10-6 M) for 25 min before and during tetanic stimulation of the mossy fibers, whereas the basal amplitude of population spikes before tetanus was hardly affected by the drug. The dose-response curve was bell-shaped with a maximal augmentation at 10-7 M. Scopolamine (10-6 M) per se had little effect on the magnitude of LTP in the mossy fiber-CA3 pathway, but significantly attenuated its enhancement by FK960 (10-7 M). In hippocampal slices from animals treated with cysteamine (200 mg/kg, s.c.), which was shown to deplete the hippocampal somatostatin, FK960 (10-7 M) hardly affected the LTP. These results suggest that FK960 enhances the magnitude of LTP in the mossy fiber-CA3 pathway through an activation of the cholinergic-somatostatinergic link in the hippocampal formation. Furthermore, it can be postulated that the drug regulates the cognitive function by modulating directly synaptic plasticity in the hippocampal neuronal network.
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PMID:FK960, a novel potential anti-dementia drug, augments long-term potentiation in mossy fiber-CA3 pathway of guinea-pig hippocampal slices. 962 44

Our previous studies demonstrated that huperzine A, a reversible and selective acetylcholinesterase inhibitor, exerts beneficial effects on memory deficits in various rodent models of amnesia. To extend the antiamnesic action of huperzine A to nonhuman primates, huperzine A was evaluated for its ability to reverse the deficits in spatial memory produced by scopolamine in young adult monkeys or those that are naturally occurring in aged monkeys using a delayed-response task. Scopolamine, a muscarinic receptor antagonist, dose dependently impaired performance with the highest dose (0.03 mg/kg, i.m.) producing a significant reduction in choice accuracy in young adult monkeys. The delayed performance changed from an average of 26.8/30 trials correct on saline control to an average of 20.2/30 trials correct after scopolamine administration. Huperzine A (0.01-0. 1 mg/kg, i.m.) significantly reversed deficits induced by scopolamine in young adult monkeys on a delayed-response task; performance after an optimal dose (0.1 mg/kg) averaged 25.0/30 correct. In four aged monkeys, huperzine A (0.001-0.01 mg/kg, i.m.) significantly increased choice accuracy from 20.5/30 on saline control to 25.2/30 at the optimal dose (0.001 mg/kg for two monkeys and 0.01 mg/kg for the other two monkeys). The beneficial effects of huperzine A on delayed-response performance were long lasting; monkeys remained improved for about 24 h after a single injection of huperzine A. This study extended the findings that huperzine A improves the mnemonic performance requiring working memory in monkeys, and suggests that huperzine A may be a promising agent for clinical therapy of cognitive impairments in patients with Alzheimer's disease.
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PMID:Improving effects of huperzine A on spatial working memory in aged monkeys and young adult monkeys with experimental cognitive impairment. 991 93

The effects of three K(+) channel blockers, 4-aminopyridine, 3, 4-diaminopyridine and apamin, on scopolamine- or electroconvulsive shock-induced amnesia were investigated in mice by using a one-trial step-down passive avoidance system. Scopolamine and electroconvulsive shock reduced the retention latency of passive avoidance, which indicated the amnestic effect of these treatments. 4-Aminopyridine, 3,4-diaminopyridine and apamin injected immediately after the acquisition trial, reversed the amnestic effect of scopolamine or electroconvulsive shock in a dose-dependent manner. None of the drugs or electroconvulsive shock treatment affected the rotarod or activity cage performance of the mice. These results indicate that K(+) channel blockers may improve cognitive deficits when memory is impaired by a drug or any other manipulation.
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PMID:The effects of some K(+) channel blockers on scopolamine- or electroconvulsive shock-induced amnesia in mice. 1105 Mar 3

Effects of 2-[2-(1-benzylpiperidin-4-yl)ethyl]-2,3-dihydro-9-methoxy-1H-pyrrolo[3,4-b]quinolin-1-one hemifumarate (T-82), a new quinoline derivative, on drug- and basal forebrain lesion-induced amnesia models were examined in rats. Scopolamine (0.5 mg/kg, i.p.) and cycloheximide (1.5 mg/kg, s.c.) shortened the step-through latency in the passive avoidance task. T-82 significantly ameliorated amnesia induced by scopolamine or cycloheximide at the dose of 0.03, 0.1 and 0.3 mg/kg, p.o., and 0.3 and 1.0 mg/kg, p.o., respectively. Basal forebrain lesions with ibotenic acid shortened the step-through latency in passive avoidance task. An acute (0.1 and 0.3 mg/kg, p.o.) or subacute (0.03-0.3 mg/kg, p.o., for 7 days) treatment of T-82 significantly reversed the shortened latency. These results suggest that T-82 may ameliorate the impairment of memory induced by acetylcholinergic dysfunction.
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PMID:Effects of T-82, a novel acetylcholinesterase inhibitor, on impaired learning and memory in passive avoidance task in rats. 1265 Aug 38

Pramiracetam has been evaluated for its potential antiamnesic properties in scopolamine-induced amnesia in healthy volunteers. Two groups of twelve males, 18-42 and 55-65 years old, respectively, were randomly assigned to oral treatment with pramiracetam (600 mg twice a day) or with placebo for 10 consecutive days. On day 11 each subject was injected intramuscularly with scopolamine hydrobromide (0.5 mg). Before scopolamine injection and then 1, 3 and 6 h after it, subjects were administered the following psychometric tests: simple and choice visual reaction times, digit symbol substitution test, Rey's 15 words test for short and long term verbal memory. Scopolamine significantly impaired episodic memory and selective attention tests in both scopolamine and placebo groups. Instead visuo-motor and incidental learning measures were unaffected. Pramiracetam, when compared to placebo, was able to partially reduce the amnesic effects induced by scopolamine both in young and old subjects.
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PMID:Pramiracetam effects on scopolamine-induced amnesia in healthy volunteers. 1537 6


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