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

Effects of MCI-225, [4-(2-fluorophenyl)-6-methyl-2-(1-piperazinyl)thieno[2,3-d]pyrimidine monohydrate hydrochloride] on experimental amnesia were studied in rats and compared with those of THA [9-amino-1,2,3,4-tetrahydroacridine]. In the Morris-type water maze task, MCI-225 (1-10 mg/kg, PO) reduced the spatial learning impairment induced by scopolamine (0.5 mg/kg, IP). In a passive avoidance (PA) task, administration of MCI-225 prior to training (1-30 mg/kg, PO) lessened the carbon dioxide (CO2)-induced amnesia in a dose-dependent manner. MCI-225 (1-100 mg/kg) did not affect gross behavior. THA (0.1-3 mg/kg, PO) reduced scopolamine-induced learning deficits in the water maze task, but the effect was not significant. THA (0.3-3 mg/kg, PO) also ameliorated the CO2-induced amnesia, although slightly, in the PA task. THA (10 mg/kg, PO) increased locomotor activity and higher dose of THA (30 mg/kg, PO) induced tremor, hypersalivation, and muscle relaxation. These results suggest that MCI-225 lessens impairments in learning and memory without causing serious behavioral abnormalities.
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PMID:Effects of a novel compound MCI-225 on impaired learning and memory in rats. 809 Aug

We investigated the effects of vinconate, a novel indolonaphthylidine derivative, on maze performance deficits induced by an electrolytic lesion of the basal forebrain (BF) in rats. Bilateral BF lesions were produced by passing an anodal DC current (2 mA, 20 s). In the BF-lesioned groups, the latency and distance that the rat swam to escape onto the platform during training in Morris's water maze task significantly increased. Vinconate (5 and 10 mg/kg) treatment shortened the increase of escape latency to the platform in the BF-lesioned rats. The electrolytic BF lesion caused marked reductions of the contents of monoamines and their metabolites in the fronto-parietal cortex, hippocampus and striatum, while it slightly decreased choline acetyltransferase activity in the fronto-parietal cortex, but not significantly. Vinconate treatment showed a tendency to reverse the decreases of serotonin in the fronto-parietal cortex and hippocampus and dopamine in the striatum. Moreover, the reductions of their metabolites were also slightly attenuated by vinconate. These data suggest that vinconate has an anti-amnesic effect on the electrolytic BF lesion-induced amnesia by partly ameliorating the dysfunction in monoaminergic neurons.
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PMID:Effects of vinconate on maze performance deficit induced by monoaminergic dysfunction in rats. 809 Oct 3

Nerve growth factor plays an important role in the survival and maintenance of cholinergic neurons in the central neuronal system. In senile dementia of the Alzheimer type, learning and memory are impaired by the loss of neurons in the magnocellular cholinergic neuronal system. It is, therefore, of interest to investigate the role of nerve growth factor in senile dementia of the Alzheimer type. We now found that 6-(4-hydroxybutyl)-2,3,5-trimethyl-1,4- benzoquinone (TMQ) stimulates nerve growth factor synthesis in mouse astroglial cells and that the compound has improving effects on memory and choline acetyltransferase activity in basal forebrain-lesioned rats, an amnesia animal model. TMQ ameliorated amnesia in the water maze and passive avoidance tasks. The compound not only restored the reduced choline acetyltransferase activity in the parietal cerebral cortex, but also increased nerve growth factor content and choline acetyltransferase activity in the hippocampus, although it did not change either of these parameters in any brain region in intact rats. These results suggest that the compound activates cholinergic neurons only in the damaged brain and, further, indicate that nerve growth factor stimulators could be used in clinical trials for the treatment of senile dementia of the Alzheimer type.
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PMID:Effects of oral administration of a stimulator for nerve growth factor synthesis in basal forebrain-lesioned rats. 811 22

In our previous study, bolus injection of VIP into the lateral cerebral ventricle, at nonphysiological high doses, has been shown to produce amnesia. Accordingly, in the present study, VIP was infused chronically into the cerebral ventricle of the rat at a rate of 10 ng per day for 2 weeks. During the infusion period, the animals were subjected to the Morris water pool test. The VIP infusion caused an apparent impairment of memory, particularly in the acquisition of new information; VIP(1-12) also caused similar impairment, but to a lesser extent. The VIP antagonists did not affect the performance of learned tasks. However, cerulein treatment prevented the VIP-induced memory impairment.
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PMID:Influence of chronic intracerebroventricular infusion of vasoactive intestinal peptide (VIP) on memory processes in Morris water pool test in the rat. 828 59

The effects of repeated propentofylline administration on impairments of learning and memory in rats with basal forebrain lesions were investigated in several behavioral tasks (water maze, habituation and passive avoidance tasks). Rats were subjected to all the tasks in sequence. Basal forebrain lesions produced by bilateral injections of ibotenic acid (approximately 6 micrograms on each side) severely impaired performance in water maze, habituation and passive avoidance tasks. Repeated administration of propentofylline (10 and 25 mg/kg per day for 14 days, p.o.) improved the deficits of performance in a water maze task, even when administration began one week after the basal forebrain lesions were produced. The impaired performance in habituation and passive avoidance tasks was also markedly ameliorated after repeated administration (24 and 26 days) of propentofylline. The rats with basal forebrain lesions exhibited a significant decrease in choline acetyltransferase activity in the cortex. Propentofylline significantly increased hippocampal choline acetyltransferase activity in basal forebrain-lesioned rats compared with that in vehicle-treated basal forebrain-lesioned rats. However, cortical choline acetyltransferase activity in basal forebrain-lesioned animals was not affected by repeated propentofylline administration. These results indicate that repeated administration of this agent ameliorated the impaired performance of basal forebrain-lesioned rats in part by increasing hippocampal choline acetyltransferase activity. Propentofylline might be useful for the treatment of amnesia and dementia.
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PMID:Effects of repeated administration of propentofylline on memory impairment produced by basal forebrain lesion in rats. 835 99

The effects of a sustained-release formulation of thyrotropin-releasing hormone (TRH-SR) on learning impairments induced by scopolamine and a cholinergic neurotoxin, ethylcholine aziridinium ion (AF64A), were examined in rodents. Subcutaneous injection of TRH-SR (2.8 mg/kg as free TRH) produced a sustained increase in immunoreactive plasma TRH levels up to about 2 weeks after dosing in rats. TRH-SR (0.56 and 2.8 mg/kg) given subcutaneously 7 days before the acquisition trial markedly ameliorated scopolamine-induced amnesia in mice, as evaluated with a passive avoidance task. Repeated administration of TRH for 7 days at doses of 0.2-5 mg/kg s.c. elicited a dose-dependent recovery from amnesia induced by scopolamine, whereas only the group treated with 5 mg/kg/day showed a significant improvement. The rats with bilateral intracerebroventricular injection of AF64A (3.75 nmol/brain) showed a significant impairment in the water maze task 2 weeks after surgery. TRH-SR (0.56 and 2.8 mg/kg) also exhibited a dose-dependent ameliorating action on the deficit. These findings indicate that TRH-SR ameliorates learning impairments produced by scopolamine and AF64A, and suggest that continuous infusion of TRH may have a potent learning and memory improving action at low doses.
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PMID:Effects of sustained release formulation of thyrotropin-releasing hormone on learning impairments caused by scopolamine and AF64A in rodents. 840 91

Effects of nerve growth factor (NGF) on the basal forebrain (BF) lesion-induced amnesia in rats were investigated. When NGF infusion was begun immediately after the formation of BF lesions, NGF ameliorated amnesia in a water maze task and showed a tendency to increase choline acetyltransferase (CAT) activity in the fronto-parietal cortex. The amnesia and the decrease of CAT activity were not ameliorated when NGF infusion was begun 4 weeks after BF lesion formation. These observations suggest that NGF may act as a trophic and/or a protective factor on partially damaged cholinergic neurons and that the efficacy of NGF was influenced by the phase of neuronal damage.
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PMID:Effects of nerve growth factor (NGF) in rats with basal forebrain lesions. 845 51

Passive avoidance training has been shown to cause an increase in synaptic density (Nvsyn) in the lobus parolfactorius (LPO) of the one-day old chick. The present study was conducted to investigate the time-course over which this plastic change takes place. Two groups of chicks were trained to peck at either a water coated bead (Control) or a methyl-anthranilate coated bead (M-trained). M-trained chicks showed avoidance responses when offered a similar but dry bead, 30 min later. Right and left hemisphere LPOs were obtained at intervals of 1, 6, 12, 24 and 48 h after training. Synaptic counts were made using a 3-dimensional stereological probe; the 'dissector'. A significantly larger mean Nvsyn (31%) was found in the left hemisphere of M-trained chicks 24 h after training, compared with Control chicks, and the difference fell to 10% at 48 h post-training. M-trained chicks also had a greater Nvsyn (17%) in the right hemisphere at 48 h post-training. The bilaterality of these findings is of particular interest, since unilateral lesions of the LPO fail to produce amnesia for the avoidance task. The importance of these results in the process of memory formation is discussed.
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PMID:Long-term increases in the numerical density of synapses in the chick lobus parolfactorius after passive avoidance training. 848 74

Head trauma leading to concussion and electroconvulsive shock (ECS) in humans causes amnesia for events that occurred shortly before the injury (retrograde amnesia). The present experiment investigated the amnesic effect of lidocaine and ECS in 25 rats trained on a working memory version of the Morris water task. Each day, the escape platform was moved to a new location; learning was evidenced by a decrease in the latency to find the platform from the first to the second trial. "Consolidation" of this newly encoded spatial engram was disrupted by bilateral inactivation of the dorsal hippocampus with 1 microliter of 4% lidocaine applied as soon as possible after the first trial. When trial 2 was given after recovery from the lidocaine (30 min after the injection), a normal decrease in latency indicated that the new engram was not disrupted. When trial 2 was given under the influence of lidocaine (5 min after injection), absence of latency decrease demonstrated both the success of the inactivation and the importance of hippocampus for the task. To examine the role of events immediately after learning, ECS (30 or 100 mA, 50 Hz, 1.2 sec) was applied 0 sec to 45 sec after a single escape to the new platform location. A 2-h delay between ECS and trial 2 allowed the effects of ECS to dissipate. ECS applied 45 sec or 30 sec after trial 1 caused no retrograde amnesia: escape latencies on trial 2 were the same as in control rats. However, ECS applied 0 sec or 15 sec after trial 1 induced clear retrograde amnesia: escape latencies on trial 2 were no shorter than on trial 1. It is concluded that the consolidation of a newly formed memory for spatial location can only be disrupted by ECS within 30 sec after learning.
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PMID:Electroconvulsive shock and lidocaine reveal rapid consolidation of spatial working memory in the water maze. 863 8

Substantial evidences suggest that the increased cerebral deposition, and neurotoxic action of the beta-amyloid peptide, the major constituent of senile plaques, may represent the underlying cause of the cognitive deficits observed in Alzheimer's disease. Herein, we attempted to verify this hypothesis by inducing a potential Alzheimer's-type amnesia after direct intracerebroventricular administration of aggregated beta 25-35-amyloid peptide in mice. In this aim, mnesic capacities were evaluated after 6-13 days, using spontaneous alternation in the Y-maze, step-down type passive avoidance and place learning in a water-maze. Pretraining administration of aggregated beta 25-35 peptide induced dose-dependent decreases in both alternation behaviour and passive avoidance, at doses of 3 and 9 nmol/mouse. A reduced but still significant impairment was observed when the peptide was not aggregated, or 'aged', by preincubation for 4 days at 37 degrees C. The beta 1-28 peptide, at 3 nmol/mouse, also induced a marked decrease in step-down latency. Posttraining, but not preretention, administration of beta 25-35 peptide also significantly impaired learning. The beneficial effects of cholinergic agents on beta 25-35-induced amnesia was examined using the cholinesterase inhibitor tacrine (THA, 1.3 and 4.3 mumol/kg i.p.) and the nicotinic receptor agonist (-)-nicotine (NIC, 0.06 and 0.2 mumol/kg i.p.). Both drugs induced a dose-dependent abrogation of the beta 25-35-induced decreases in alternation behaviour and passive avoidance. Furthermore, THA, at 1.3 mumol/kg, and NIC, at 0.2 mumol/kg, also reversed the beta 25-35-induced impairment of place learning and retention in the water-maze. Histological examination of Cresyl violet-stained brain sections indicated a moderate but significant cell loss within the frontoparietal cortex and the hippocampal formation of mice treated with aged beta 25-35 peptide (9 nmol). Examination of Congo red-stained sections in the same animals demonstrated the presence of numerous amyloid deposits throughout these brain areas. These results confirm that the deposition of beta-amyloid peptide in the brain is in some way related to impairment of learning and cholinergic degeneration and suggest that the [25-35] fragment of the beta-amyloid protein, sufficient to induce neuronal death in cultures, also induces an Alzheimer's-type amnesia in mice.
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PMID:Amnesia induced in mice by centrally administered beta-amyloid peptides involves cholinergic dysfunction. 882 55


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