Effect of centrally administered atropine and pirenzepine on radial arm maze performance in the rat

Sala, Mariaelvina; Braida, Daniela; Calcaterra, P.; Leone, M.P.; Comotti, F; Gianola, Silvia; Gori, E

doi:10.1016/0014-2999(91)90122-7

Cited by 53 publications

(19 citation statements)

References 23 publications

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“…Studies using pharmacological antagonists and brain lesions have indicated that the disturbance of central cholinergic transmission is associated with cognitive impairment (9,10). In the present study a cholinergic receptor antagonist scopolamine that is widely accepted as an agent causing cognitive deficits in experimental animals with induced performance impairment in both passive avoidance and radial-arm maze tasks, in agreement with the previous reports (5,11).…”

supporting

confidence: 91%

Ameliorative Effects of Azaindolizinone Derivative ZSET845 on Scopolamine-Induced Deficits in Passive Avoidance and Radial-Arm Maze Learning in the Rat

Yamaguchi

Higashi

Matsuno

et al. 2001

Japanese Journal of Pharmacology

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ABSTRACT-Effects of ZSET845 (3,3-dibenzylimidazo[1,2-a]pyridin-2-(3H)-one), a newly synthesized cognitive enhancer, and donepezil and tacrine on the scopolamine-induced cognitive deficits in rats were examined in passive avoidance and radial-arm maze tasks. ZSET845 (0.01 mg/kg) showed a greater ameliorative effect than donepezil (0.1 mg/kg) or tacrine (1 mg/kg) in the passive avoidance task. In the radial-arm maze task, ZSET845 (0.1 mg/ kg) also showed a greater effect than donepezil (10 mg/kg) or tacrine (10 mg/ kg). ZSET845 induced an increase in the choline acetyltransferase (ChAT) activity in the hippocampus, suggesting that the ameliorative effects of ZSET845 are related to the increase in the ChAT activity in the hippocampus.

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supporting

confidence: 91%

Ameliorative Effects of Azaindolizinone Derivative ZSET845 on Scopolamine-Induced Deficits in Passive Avoidance and Radial-Arm Maze Learning in the Rat

Yamaguchi

Higashi

Matsuno

et al. 2001

Japanese Journal of Pharmacology

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“…A delay-dependent disruption following treatment with scopolamine and atropine, that appeared to resemble that occurring spontaneously in aged subjects and in Alzheimer patients, has been reported (Duetsch, 1971;Bartus and Johnson, 1976). Animals treated with the M 1 selective antagonist pirenzepine (Hammer et al, 1980), had impaired passive avoidance learning (in mice) (Caufield et al, 1983) and impaired spatial learning (Hagan et al, 1987;Hunter and Roberts, 1988), radial arm maze performance (Sala et al, 1991) and active avoidance acquisition (Sen and Bhattacharya, 1991) in rats. Moreover, the M 1 selective antagonists dicyclomine (Nilvebrant and Sparf, 1986) and S-(−)-ET-126 (Ghelardini et al, 1996) were able to induce amnesia in a mouse passive avoidance task (Ghelardini et al, 1997b;Matucci et al, 1997).…”

Section: Introductionmentioning

confidence: 98%

Antisense ‘knockdowns’ of M1 receptors induces transient anterograde amnesia in mice

et al. 1999

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The effect on memory processes of inactivation of the M 1 gene by an antisense oligodeoxyribonucleotide (aODN) was investigated in the mouse passive avoidance test. Mice received a single intracerebroventricular (i.c.v.) injection of M 1 aODN (0.3, 1.0 or 2.0 nmol per injection), degenerated ODN (dODN) or vehicle on days 1, 4 and 7. An amnesic effect, comparable to that produced by antimuscarinic drugs, was observed 12, 24, 48 and 72 h after the last i.c.v. aODN injection, whereas dODN and vehicle, used as controls, did not produce any effect. Reduction in the entrance latency to the dark compartment induced by aODN disappeared 7 days after the end of aODN treatment, which indicates the absence of any irreversible damage or toxicity caused by aODN. Quantitative reverse transcription-polymerase chain reaction analysis demonstrated that a decrease in M 1 mRNA levels occurred only in the aODN-treated group, being absent in all control groups. Furthermore, a reduction in M 1 receptors was observed in the hippocampus of aODN-treated mice. Neither aODN, dODN nor vehicle produced any behavioral impairment of mice. These results indicate that the integrity and functionality of M 1 receptors are fundamental in the modulation of memory processes.

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“…The administration of scopolamine, an unselective muscarinic ACh receptor antagonist, results in impaired learning and memory in humans [Frumier et al, 1976] and animals [Levin and Bowman 1986]. Animals treated with the M 1 selective antagonist pirenzepine and dicyclomine had impaired memory processes in various paradigms in both mice and rats [Caufield et al, 1983;Sala et al, 1991;Ghelardini et al, 1997]. Furthermore, the administration of nicotinic ACh receptor antagonists, such as mecamylamine, produces a dose-dependent impairment of performance in the passive avoidance test [Elrod and Buccafusco, 1981].…”

Section: Discussionmentioning

confidence: 99%

The novel nootropic compound DM232 (UNIFIRAM) ameliorates memory impairment in mice and rats

Ghelardini

Galeotti

Gualtieri

et al. 2002

Drug Development Research

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The favorable pharmacological profile exhibited by piracetam stimulated the synthesis of related compounds potentially endowed with a higher nootropic potency. The antiamnesic and procognitive activity of DM232 (unifiram), a new compound structurally related to piracetam, was investigated. Mouse passive avoidance and rat Morris water maze and Social learning tests were employed. DM232 (0.001-1 mg kg À1 i.p. -0.01-0.1 1 mg kg À1 p.o.) prevented amnesia induced by scopolamine (1.5 mg kg À1 i.p.), mecamylamine (20 mg kg À1 i.p.), baclofen (2 mg kg À1 i.p.), and clonidine (0.125 mg kg À1 i.p.). Furthermore, The antiamnesic effect of the investigated compound was comparable to that exerted by well-known nootropic drugs such as piracetam (30-100 mg kg À1 i.p.), aniracetam (100 mg kg À1 p.o.), rolipram (30 mg kg À1 p.o.), and nicotine (5 mg kg À1 i.p). DM232 (0.1 mg kg À1 i.p.) was also able to prevent amnesia induced by scopolamine (0.8 mg kg À1 i.p.) in the rat Morris watermaze test. In the rat social learning test, DM232 (0.1 mg kg À1 i.p.) injected in adults rats reduced the duration of active exploration of the familiar partner in the second session of the test. DM232, similarly to piracetam, reduced the duration of hypnosis induced by pentobarbital. At the highest effective doses, the investigated compound did not impair motor coordination (rota rod test), nor modified spontaneous (Animex). These results indicate DM232 (unifiram) as a novel cognition enhancer, strictly related to piracetam-like compounds, able to ameliorate memory impairment at doses about 1,000 times lower than the most active available nootropic compounds. Drug Dev.

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Effect of centrally administered atropine and pirenzepine on radial arm maze performance in the rat

Cited by 53 publications

References 23 publications

Ameliorative Effects of Azaindolizinone Derivative ZSET845 on Scopolamine-Induced Deficits in Passive Avoidance and Radial-Arm Maze Learning in the Rat

Ameliorative Effects of Azaindolizinone Derivative ZSET845 on Scopolamine-Induced Deficits in Passive Avoidance and Radial-Arm Maze Learning in the Rat

Antisense ‘knockdowns’ of M1 receptors induces transient anterograde amnesia in mice

The novel nootropic compound DM232 (UNIFIRAM) ameliorates memory impairment in mice and rats

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