Memory facilitation with posttrial injection of oxotremorine and physostigmine in mice

Baratti, Carlos M.; Huygens, Patricia; Miño, Jorge; Merlo, Alicia; Gardella, Javier

doi:10.1007/bf00427350

Cited by 108 publications

(30 citation statements)

References 17 publications

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“…Anti cholinergic drugs such as scopolamine produce memory impairment in experimental animals and humans and cholinomimetics such as physostigmine, oxotremorine and arecoline enhance memory function and antagonize the memory impairments induced by scopolamine (22)(23)(24)(25). In the present experiment, however, a marked memory deficit occurred when monoaminergic, but not cholinergic mechanisms were damaged significantly.…”

Section: Discussioncontrasting

confidence: 56%

Impairment of Memory and Changes in Neurotransmitters Induced by Basal Forebrain Lesion in Rats

Araki

Uchiyama

Kawashima

et al. 1986

Japanese Journal of Pharmacology

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Abstract-The effect of bilateral electrolytic lesioning of the anterior and posterior parts of the basal forebrain (BF) on learning behavior and changes in neurotrans mitters in the central nervous system was investigated in rats. The posterior BF lesion caused more severe impairment than the anterior BF lesion in the acquisition of conditioned avoidance response in a two-way shuttle box. A severe deficit in acquisition of passive avoidance response was produced by the posterior BF lesion. Choline acetyltransferase (CAT) activity was decreased significantly in the parietal cortex but not in the occipital cortex in anterior BF-lesioned rats. However, it was not decreased in posterior BF-lesioned rats. The contents of monoamines in the hippocampus was decreased more significantly by the posterior BF lesion than by the anterior BF lesion. These results suggest that the impairment of memory in posterior BF-lesioned rats may be related mainly to monoaminergic function rather than to cholinergic deficit.

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Section: Discussioncontrasting

confidence: 56%

Impairment of Memory and Changes in Neurotransmitters Induced by Basal Forebrain Lesion in Rats

Araki

Uchiyama

Kawashima

et al. 1986

Japanese Journal of Pharmacology

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“…Since the memory impairments induced by physical (cerebral ischemia, brain injury) or chemical (drugs, anoxic treatment) means in the mouse one-trial passive avoidance test are improved by the administration of various drugs including cholinergic drugs such as physostigmine and oxotremorine before the retention trial (28,(35)(36)(37)(38), these memory impairments are considered to be due to disturbance of the retrieval process of memory rather than of the consolidation of memory (39). In a similar experiment in mice using a light-dark box, the shortened latency in the retention trial 24 hours after exposure to CO-, gas immediately following the acquisition trial was dose-dependently prolonged by oral administration of TA-0910 60 min before the retention trial.…”

Section: Discussionmentioning

confidence: 99%

“…For example, anticholinergic drugs such as scopolamine produce memory impairment in humans and experimental animals, while cholinomimetics such as physostigmine, oxotremorine and arecoline enhance memory formation (21)(22)(23)(24). We have already reported that the effects of TA-0910 on the CNS is considered to be partly mediated by activation of the cholinergic neurons (20,25).…”

mentioning

confidence: 99%

Pharmacological study of TA-0910, a new thyrotropin-releasing hormone(TRH) analog. (IV). Effects on experimental memory impairment in mice and rats.

Yamamura¹,

Kawakami²,

Nakagawa³

et al. 1991

Jpn.J.Pharmacol

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ABSTRACT-The effects of a new TRH analog, TA-0910, orally administered, on experimental memory impairments for the one-trial passive avoidance response in anoxic mice (light-dark box), active avoidance response in basal forebrain (BF)-lesioned rats (shuttle box), and delayed alternation task in scopolamine-treated rats (T-maze) were studied. In mice, TA-0910 (3 -30 mg) administered 60 min before the retention trial dose-dependently prolonged the passive avoidance response latency reduced by C02-exposure that was given immediately after the acquisition trial, but not when it was given 60 min before the acquisition or just after the anoxic treatment. In rats, TA-0910 (0.3-3 mg/kg) administered 40-60 min before the test trial, dose-dependently prevented the reduction in mean avoidance rate caused by BF-lesioning and elevated the scopolamine (0.1 mg/kg, i.p.)-induced reduction in percent correct choice level in the alternation task. TRH (30 -300 mg/kg), on the other hand, produced no improvements in any of the above tests. These results suggest that TA-0910 improves impaired memory by correcting the retrieval process of memory.Thyrotropin-releasing hormone (TRH) is a hypothalamic hormone that stimulates secretion of thyrotropin and prolactin. However, radioimmunoassay has demonstrated that twothirds of the total TRH content of the brain is distributed widely in areas other than the hypothalamus (1). Also, autoradiographic studies have revealed that TRH receptors of the brain are concentrated in the cerebral cortex and the limbic system (2, 3). Based on these findings, TRH is considered to play an important role in the brain in the maintenance of consciousness and emotional or intellectual functions (4). Moreover, Yarbrough and Pomara (5) recommended the use of TRH for the treatment of dementia of the Alzheimer type (DAT) from the functional relationship between TRH and central cholinergic nervous system and the effectiveness of TRH in the treatment of dementia of patients with amyotrophic lateral sclerosis complicated by degeneration of cholinergic nerves, and by Metcalf (6) and Griffiths (7) from the effect of TRH to improve disturbance of consciousness (8) and its antidepressant effect (9, 10).Recently, improvements in mental symptoms (such as disturbances in impressibility, emotional disturbances, reduced ability to think, deduced spontaneity, inertia, and apathy) were reported in patients with Alzheimer's disease (AD) and cerebrovascular dementia after administration of TRH (11,12). Tem-

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“…The administration of scopola mine, a muscarinic acetylcholine receptor antagonist, produces amnesic effects (21 23), while cholinergic drugs, including muscarinic agonists and acetylcholinesterase inhibitors, accelerate learning and memory in both hu mans and animals (22,24,25). The most strik ing and consistent change in AD and SDAT is in the cholinergic system, as measured by a marked decrease in choline acetyltransferase activity in the hippocampus and cerebral cor tex (8,9).…”

Section: Discussionmentioning

confidence: 99%

Working and Reference Memory in Rats in the Three-Panel Runway Task Following Dorsal Hippocampal Lesions.

et al. 1992

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Using a three-panel runway task, the influence of dorsal hippocampal lesions on working and reference memory in rats was investigated. Despite 20 postop erative training sessions, rats with hippocampal lesions were unable to perform the working memory task. In the acquisition process of the reference memory task, however, there was no significant difference between hippocampal and sham-lesioned rats. On the other hand, rats trained preoperatively with a working memory proce dure, and then subjected to hippocampal lesions, showed more errors (pushes made on the two incorrect panels of the three panel-gates located at four choice points) than did sham-lesioned rats. The increase in working errors induced by hippocampal lesions was not reduced during 10 subsequent re-training sessions. Hippocampal le sions had no effect on retention of the reference memory performance. The increase in working errors in hippocampal-lesioned rats was significantly reduced by treatment with the cholinesterase inhibitor physostigmine at 0. 1 mg/kg and the cholinergic acti vating drug minaprine at 10 mg/kg. These findings suggest that lesions of the dorsal hippocampus selectively impair the ability to carry out the working memory task whether rats are trained preoperatively or postoperatively, and that the working mem ory loss in hippocampal-lesioned rats is mediated by lowering of the cholinergic func tion.

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Memory facilitation with posttrial injection of oxotremorine and physostigmine in mice

Cited by 108 publications

References 17 publications

Impairment of Memory and Changes in Neurotransmitters Induced by Basal Forebrain Lesion in Rats

Impairment of Memory and Changes in Neurotransmitters Induced by Basal Forebrain Lesion in Rats

Pharmacological study of TA-0910, a new thyrotropin-releasing hormone(TRH) analog. (IV). Effects on experimental memory impairment in mice and rats.

Working and Reference Memory in Rats in the Three-Panel Runway Task Following Dorsal Hippocampal Lesions.

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