Lurasidone (SM-13496), a novel atypical antipsychotic drug, reverses MK-801-induced impairment of learning and memory in the rat passive-avoidance test

Ishiyama, Takeo; Tokuda, Kumiko; Ishibashi, Tadashi; Ito, Akira; Toma, Satoko; Ohno, Yukihiro

doi:10.1016/j.ejphar.2007.06.058

Cited by 143 publications

(81 citation statements)

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“…The animals were given only one intraperitoneal (ip) injection (acute treatment) or one injection per day for 5 d (subchronic treatment) as a 0.1 mL/10 g body weight dose. The doses were chosen based on previous reports about the behavioral effects of aripiprazole [4] . To study the effect that aripiprazole has on memory, the animals received injections 30 min before training in the inhibitory avoidance task.…”

Section: Drugs and Pharmacological Proceduresmentioning

confidence: 99%

“…Several studies have assessed physiopathologic aspects linked to schizophrenia, such as declarative and nondeclarative memory functions, to identify areas of impairment versus preservation [3] . Similarly, some investigations have evaluated the effect of antipsychotic drugs on cognitive parameters in humans and animals [4,5] . Research suggests that schizophrenic patients treated with atypical antipsychotics may perform better in cognitive tasks when compared to patients treated with typical antipsychotics [2,6] .…”

Section: Introductionmentioning

confidence: 99%

“…Aripiprazole, 7-{4-[4-(2,3-dichlorophenyl)-1-piperazinyl] butyloxy}-3,3-dihydro-carbostycil (Figure 1), is an atypical antipsychotic drug with distinct properties compared to other efficient antipsychotics [4] . The drug was developed recently, and it presents a unique pharmacological profile that includes dopamine D 2 partial agonism, serotonin 5-HT 1A partial agonism, and 5-HT 2A antagonism [5,6] .…”

Section: Introductionmentioning

confidence: 99%

“…In the same study, aripiprazole antagonized amphetamine-(2 mg/kg) or ethanol-induced (1.75 g/kg) locomotor stimulation [21] . Therefore, aripiprazole attenuated LY-341495-induced hyperactivity, a metabotropic glutamate receptor antagonist [20] .Another study reported that aripiprazole was able to decrease total locomotor activity in a dose-dependent manner, causing marked locomotor suppression 1 h after oral treatment with 0.3 and 1 mg/kg doses [4] . In the same work, aripiprazole was administered for 7 d, and the locomotor activity was recorded 24 h after the last treatment.…”

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confidence: 96%

“…The action mechanism of aripiprazole has not been fully clarified, which may hinder the interpretation of the data obtained in the present study. Serotonin 5-HT 1A and 5-HT 2A receptors are suggested to play important roles in cognitive functions [4] . Therefore, the effects on memory shown here might be involved in the actions of aripiprazole on those receptors.…”

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Neurobehavioral and genotoxic parameters of antipsychotic agent aripiprazole in mice

et al. 2011

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Aim: Aripiprazole is an antipsychotic agent to treat schizophrenia, which acts through dopamine D 2 partial agonism, serotonin 5-HT 1A partial agonism and 5-HT 2A antagonism. This study was designed to evaluate the neurobehavioral effects and genotoxic/mutagenic activities of the agent, as well as its effects on lipoperoxidation. Methods: Open field and inhibitory avoidance tasks were used. Thirty min before performing the behavioral tasks, adult male CF-1 mice were administered aripiprazole (1, 3 or 10 mg/kg, ip) once for the acute treatment, or the same doses for 5 d for the subchronic treatment. Genotoxic effects were assessed using comet assay in the blood and brain tissues. Mutagenic effects were evaluated using bone marrow micronucleus test. Lipoperoxidation was assessed with thiobarbituric acid reactive substances (TBARS). Results: Acute and subchronic treatments significantly decreased the number of crossing and rearing in the open field task. Acute treatment significantly increased the step-down latency for both the short-and long-term memory in the inhibitory avoidance task. Subchronic treatments with aripiprazole (3 and 10 mg/kg) caused significant DNA strain-break damage in peripheral blood but not in the brain. Mutagenic effect was not detected in the acute and subchronic treatments. Nor TBARS levels in the liver were affected. Conclusion: Aripiprazole improved memory, but could impair motor activities in mice. The drug increased DNA damage in blood, but did not show mutagenic effects, suggesting that it might affect long-term genomic stability.Keywords: antipsychotic agent; aripiprazole; locomotion; memory; genotoxic/mutagenic activities; DNA damage; lipoperoxidation Acta Pharmacologica Sinica (2011Sinica ( ) 32: 1225Sinica ( -1232 doi: 10.1038/aps.2011 published online 15 Aug 2011 Original Article * To whom correspondence should be addressed. [8] .In the experimental context, Nagai et al [9] showed that aripiprazole that was administered as either a single dose or as consecutive doses (for 7 d) ameliorated phencyclidine-induced impairment of recognition memory in mice. However, another study showed that aripiprazole impaired the passiveavoidance response at doses near its anti-dopamine ED 50 (7.7 mg/kg, as defined by apomorphine stereotypy). At doses lower than those that affected the passive-avoidance response, aripiprazole was unable to reverse the MK-801-induced impairment in the same task [4] . Therefore, further investigations are necessary to elucidate the effect of aripiprazole on memory.The aim of the present study was to investigate the effects of aripiprazole on memory and on locomotor and exploratory activities with the inhibitory avoidance and open field tasks as behavioral models. Some drugs that affect memory can induce damage in biomolecules, such as lipids and DNA. Therefore, possible cytotoxic and genotoxic effects were evaluated by measuring lipid peroxidation in the liver and DNA strand breaks in both the peripheral blood and brain tissues after behavioral tasks. Mutagenic e...

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Section: Drugs and Pharmacological Proceduresmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 96%

mentioning

confidence: 99%

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Neurobehavioral and genotoxic parameters of antipsychotic agent aripiprazole in mice

et al. 2011

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Antipsychotic Drugs

et al. 2015

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Alkylation, Annulation, and Alkenylation of Organic Molecules with Maleimides by Transition‐Metal‐Catalyzed C‐H Bond Activation

2019

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Maleimide and succinimide core moieties are present in various natural products and pharmaceuticals. In addition, these derivatives can be readily modified into biologically important organic molecules including pyrrolidines and γ-lactams. A transition-metal-catalyzed chelationassisted functionalization of inert CÀ H bond of organic molecules with electrophiles or nucleophiles is one of the efficient methods to construct chemical bonds in a highly atom-and step-economical manner. The present review describes the recent advances in the reaction involving maleimides with organic molecules by a chelation-assisted inert CÀ H bond activation methodology. The reaction involving maleimides with organic molecules having directing groups, such as ketone, acyl, pyridyl, pyrimidyl, oxime, amide, imidate, chromone, azo, N-sulfonyl ketimine, carboxylic acids, and aldimines, were described. The scope, limitation and mechanistic investigation of the alkylation, annulation and alkenylation reactions were discussed elaborately. This review article includes the entire report on the chemical bondforming reaction of maleimides with organic molecules by the CÀ H bond activation strategy until the end of 2018.

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Lurasidone (SM-13496), a novel atypical antipsychotic drug, reverses MK-801-induced impairment of learning and memory in the rat passive-avoidance test

Cited by 143 publications

References 50 publications

Neurobehavioral and genotoxic parameters of antipsychotic agent aripiprazole in mice

Neurobehavioral and genotoxic parameters of antipsychotic agent aripiprazole in mice

Antipsychotic Drugs

Alkylation, Annulation, and Alkenylation of Organic Molecules with Maleimides by Transition‐Metal‐Catalyzed C‐H Bond Activation

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