Action of nootropic drugs on transcallosal responses in rats

Okuyama, Shigeru; Aihara, Hironaka

doi:10.1016/0028-3908(88)90202-x

Cited by 27 publications

(8 citation statements)

References 36 publications

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“…Although the mechanism of action of nootropics on memory formation is unknown, these compounds have been shown to facilitate the transcollosal, interhemispheric transfer of information (Okuyama and Aihara 1988) and enhance long-term potentiation (LTP) in guinea-pig hippocampal slices (Satoh et al 1986). The possible role of LTP in memory has been widely discussed (Izquierdo 1991).…”

Section: Discussionmentioning

confidence: 99%

Effects of four non-cholinergic cognitive enhancers in comparison with tacrine and galanthamine on scopolamine-induced amnesia in rats

1992

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Amnesia can be induced in rats in the passive avoidance paradigm by administration of scopolamine, a central muscarinic receptor antagonist. Tacrine or galanthamine, inhibitors of acetylcholinesterase, given in conjunction with scopolamine partially reversed the scopolamine-induced deficit in passive avoidance performance. Four so-called cognitive enhancers, all widely used for the treatment of the symptoms associated with mental aging, cerebral insufficiency and senile memory disorder, were investigated in this paradigm. Piracetam, an extract of Ginkgo biloba, dihydroergocristine and a combination of raubasine with dihydroergocristine, all attenuated the amnesia induced by scopolamine. In contrast, nicergoline had no significant effect. Raubasine alone also failed to significantly attenuate scopolamine-induced amnesia, although some doses of raubasine had a non-significant tendency (P less than 0.10) to reduce the amnesia.

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Section: Discussionmentioning

confidence: 99%

Effects of four non-cholinergic cognitive enhancers in comparison with tacrine and galanthamine on scopolamine-induced amnesia in rats

1992

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“…Moreover, bifemelane given before ischemia antagonizes learning deficits in rats (Tobe et al, 1986). Concerning bifemelane actions that may be related to cognition enhancing activity, electrophysiological studies support cholinomimetic activity (Tobe et a/., 1981; Egawa et al, 1987;Okuyama and Aihara, 1988). Another potentially important aspect for cognition enhancing activity relates to various actions in the CA3 region of the hippocampus, such as an induction of translocation of kinase C and an increase of glutamate release (Fujii et al, 1990(Fujii et al, , 1991Ueda et al, 1992) and an enhancement of long-term potentiation (LTP) efficacy (Satoh et al, 1988), which is believed to be a basic mechanism of memory formation.…”

Section: Introductionmentioning

confidence: 92%

“…Moreover, bifemelane given before ischemia antagonizes learning deficits in rats (Tobe et al, 1986). Concerning bifemelane actions that may be related to cognition enhancing activity, electrophysiological studies support cholinomimetic activity (Tobe et a/., 1981;Egawa et al, 1987;Okuyama and Aihara, 1988 The authors speculated that bifemelane may act both as a metabolic activator and a vasodilator. In a study with 10 patients with Alzheimer-type dementia and 10 patients with multi-infarct dementia, eight subjects out of 20 were regarded as responders after a 3-month treatment period with a daily dosage of 150 mg bifemelane (Shigeta et al, 1993a,b).…”

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confidence: 93%

Testing Drugs for Impaired Brain Function in Old Age: On the Effects of a Single Dose of Bifemelane using Topographic Mapping of EEG and Event-Related Potentials (P300) and Psychometric Measurements in Healthy Elderly Subjects

Semlitsch

Saletu

Anderer

et al. 1996

Hum. Psychopharmacol. Clin. Exp.

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Clinical studies have demonstrated that bifemelane hydrochloride [4-(0-benzylphenoxy)-N-methylbutylamine hydrochloride] can improve cognitive functions in patients with various types of dementia. To elucidate specific mechanisms which may underlie the clinical benefit, the effects of bifemelane were investigated by means of computerized electroencephalography (EEG), event-related potentials (P300) and psychometry. Eighteen healthy elderly subjects, aged between 60 and 73 years, were included in a double-blind, placebo-controlled crossover study. Each subject received a single dose of 150 mg bifemelane or placebo with an interval of 1 week in between. EEG and psychometric investigations were carried out before and 2, 4, 6, and 8 h after drug administration, ERP investigations only before and 3 h after drug administration. Descriptive data analysis of the EEG showed that 150 mg bifemelane accelerated the centroid of the total frequency band, induced a significant reduction of the absolute delta + theta power and increased the absolute beta power most markedly 6 h after drug intake. Topographic analyses of ERP amplitudes showed that bifemelane did not effect ERP amplitudes. While N1, P2 and N2 latencies were not changed after bifemelane, P300 latency was shortened significantly. Psychometric investigations did not show significant or consistent effects on noopsychic and thymopsychic functions. In conclusion, bifemelane affected EEG in the sense of improved vigilance. The reduction of P300 latency may be interpreted as accelerated stimulus evaluation time, therefore indicating a beneficial effect of bifemelane on cognition at this stage of information processing. (Ogawa et al., 1992a). Moreover, bifemelane given before ischemia antagonizes learning deficits in rats (Tobe et al., 1986). Concerning bifemelane actions that may be related to cognition enhancing activity, electrophysiological studies support cholinomimetic activity (Tobe et a/., 1981;Egawa et al., 1987;Okuyama and Aihara, 1988 The authors speculated that bifemelane may act both as a metabolic activator and a vasodilator. In a study with 10 patients with Alzheimer-type dementia and 10 patients with multi-infarct dementia, eight subjects out of 20 were regarded as responders after a 3-month treatment period with a daily dosage of 150 mg bifemelane (Shigeta et al., 1993a,b). As the frequency of small rapid eye movements in the EOG increased significantly only in responders, and as only responders demonstrated a significant reduction in amplitude of the 6.0-8.0 Hz EEG frequency band, the authors concluded that part of the intellectual improvement in the patients resulted from an increased level of arousal. KEYWhile the ultimate goal in the evaluation of nootropic drugs lies in the demonstration of clinically relevant changes (Amaducci et al., 1990; Advisory Committees to the German Federal Health Office, 1992), computerized electrophysiological methods like topographic mapping of the electroencephalogram (EEG) may allow classification as well as the evaluati...

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“…The antiamnesic and memory-enhancing properties of these compounds have been demonstrated in various animal species and numerous experimental paradigms [Gouliaev and Senning, 1994]. Furthermore, these compounds facilitate the transcallosal, interhemispheric transfer of information [Okuyama and Aihara, 1988] and enhance long-term potentiation (LTP) in guinea-pig hippocampal slices [Satoh et al, 1986;Pugliese et al, 1989]. The members of this class present very low toxicity, no sedative or stimulatory effects, and lack of serious side effects of DDR Grant sponsor: MURST.…”

Section: Introductionmentioning

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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Action of nootropic drugs on transcallosal responses in rats

Cited by 27 publications

References 36 publications

Effects of four non-cholinergic cognitive enhancers in comparison with tacrine and galanthamine on scopolamine-induced amnesia in rats

Effects of four non-cholinergic cognitive enhancers in comparison with tacrine and galanthamine on scopolamine-induced amnesia in rats

Testing Drugs for Impaired Brain Function in Old Age: On the Effects of a Single Dose of Bifemelane using Topographic Mapping of EEG and Event-Related Potentials (P300) and Psychometric Measurements in Healthy Elderly Subjects

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

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