Involvement of N-methyl-D-aspartate (NMDA) receptors in noncompetitive NMDA receptor antagonist-induced hyperlocomotion in mice

Irifune, Masahiro; Shimizu, Takao; Nomoto, Masahiro; Fukuda, Takeo

doi:10.1016/0091-3057(94)00379-w

Cited by 68 publications

(29 citation statements)

References 19 publications

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“…In addition, these effects induced by memantine lasted for 3 h. As shown above, memantine had NMDA-antagonistic activity. It is well known that MK-801, a drug showing NMDAreceptor antagonistic activity, caused hyperlocomotion in rats (27). Almost identical results were obtained with NPC 12626, an NMDA-receptor antagonist, in rats (28).…”

Section: Discussionsupporting

confidence: 68%

“…2.0. The power spectrum densities, integrated and averaged, could be divided into 4 frequency areas: delta wave (0.5 -4 Hz), theta wave (4 -8 Hz), alpha wave (8 -13 Hz), and beta wave (13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30). Delta activity (%) was calculated by the following equation: Delta activity (%) = delta wave power density in the drug administration period / delta wave power density in the vehicle administration period in each animal × 100.…”

Section: Calculation Of Delta Activity During Non-rem Sleepmentioning

confidence: 99%

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Characteristic Effects of Anti-dementia Drugs on Rat Sleep Patterns

Ishida

Kamei

2009

J Pharmacol Sci

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Abstract. The present study was undertaken to clarify the effects of anti-dementia drugs on sleep pattern in rats. Electrodes were chronically implanted into the frontal cortex and the dorsal neck muscle of rats for the electroencephalogram (EEG) and electromyogram (EMG), respectively. EEG and EMG were recorded with an electroencephalograph. SleepSigh ver. 2.0 was used for analysis of the sleep-wake state. Total times of waking, non-rapid eye movement (non-REM) sleep, and rapid eye movement (REM) sleep were measured from 10:30 to 16:30. Galantamine had no significant influence on the sleep pattern. On the other hand, donepezil and memantine showed significant increases in sleep latency and total waking time and a decrease in total non-REM sleep time. Furthermore, memantine decreased total REM sleep time. To investigate the characteristics of non-REM sleep in detail, non-REM sleep was classified as stage 1, 2, or 3 according to the depth of sleep. Different from donepezil and galantamine, memantine significantly decreased stage 1 and increased stage 3 in non-REM sleep. From these findings, it can be concluded that galantamine caused no sleep disturbance, different from donepezil and memantine.

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Section: Discussionsupporting

confidence: 68%

Section: Calculation Of Delta Activity During Non-rem Sleepmentioning

confidence: 99%

Characteristic Effects of Anti-dementia Drugs on Rat Sleep Patterns

Ishida

Kamei

2009

J Pharmacol Sci

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“…The maximal scores were observed between 10 and 15 min following ketamine injection and returned to baseline values after 40 min. The time-course effect of ketamine on motor behavior in rats is similar to that previously described in mice (Irifune et al, 1995). This temporal pattern differs from those reported in rats (Druhan et al, 1996;Adams and Moghaddam, 1998) or mice (Irifune et al, 1995) with other noncompetitive NMDA antagonists, such as PCP or MK-801, which produce a longer effect with a maximal response at about 20 or 40 min postinjection, respectively.…”

Section: Discussionmentioning

confidence: 43%

“…Moreover, these compounds have been shown to exacerbate the symptomatology of schizophrenic patients (Luby et al, 1959;Lahti et al, 1995;Malhotra et al, 1997). In rodents, acute administration of PCP, ketamine or MK-801 produces hyperlocomotion and stereotypies as well as deficit in social interactions, which are thought to correspond to certain aspects of the positive and negative symptoms of schizophrenia, respectively (Irifune et al, 1995;Sams-Dodd, 1996;Adams and Moghaddam, 1998). Noncompetitive NMDA antagonists have also been found to impair performance of several cognitive tasks in rats (Butelman, 1990;Kesner and Dakis, 1993;Verma and Moghaddam, 1996) including latent inhibition, which is disrupted in patients with acute schizophrenia (Moser et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Ketamine, at a Dose that Disrupts Motor Behavior and Latent Inhibition, Enhances Prefrontal Cortex Synaptic Efficacy and Glutamate Release in the Nucleus Accumbens

Razoux

García

Léna

2006

Neuropsychopharmacol

112

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Noncompetitive N-methyl-D-aspartate (NMDA) antagonists such as ketamine represent useful pharmacological tools to model, in both healthy humans and rodents, behavioral and cerebral abnormalities of schizophrenia. These compounds are thought to exert some of their disruptive effects by impairing glutamatergic transmission in corticolimbic circuits including the nucleus accumbens (NAc). In this study, we investigated in freely moving rats behavioral changes as well as electrophysiological and neurochemical alterations in the NAc following acute systemic injection of a subanesthetic dose (25 mg/kg) of ketamine. We found that ketamine induced an immediate behavioral activation, characterized by hyperlocomotion, stereotypies and ataxia, and abolished latent inhibition in a conditioned-fear paradigm when injected at the pre-exposure stage. We also observed that during expression of motor effects which are thought to be related to the positive symptoms of schizophrenia, ketamine potentiated synaptic efficacy in the prefrontal-accumbens pathway and increased the extracellular levels of glutamate in the NAc. These results, taken together with previous findings, suggest that the psychoticlike effects of noncompetitive NMDA antagonists may be, in part, mediated by an increase in glutamate release in the NAc associated with synaptic changes in accumbens glutamatergic inputs including enhancement of synaptic efficacy in the prefrontal input.

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“…Por exemplo, antagonistas do receptor NMDA aumentam o disparo de neurônios dopaminérgicos (Murase et al, 1993) e causam liberação de dopamina neuroanatomicamente seletiva em roedores (Adams e Moghaddam, 1998;Rao et al, 1989). Em humanos, estudos de PET medindo a ocupação dos receptores dopaminérgicos após a administração de cetamina sugeriram que antagonistas NMDA aumentam a liberação de dopamina no núcleo estriado (Smith et al, 1998), e esses efeitos são suprimidos pelo menos em parte por drogas antipsicóticas (Corbett et al, 1995;Irifune et al, 1995). A cetamina mostra afinidade muito similar pelos receptores NMDA e D 2 , com menor afinidade por sítios 5HT 2 .…”

Section: Cetamina E Esquizofreniaunclassified

Cetamina: aspectos gerais e relação com a esquizofrenia

Vasconcelos¹,

Andrade²,

Soares³

et al. 2005

Rev. psiquiatr. clín.

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ResumoA cetamina é uma droga anestésica desenvolvida em 1965 pelos laboratórios norte-americanos Parke & Davis, tendo como objetivo principal sua utilização em anestesias humanas e veterinárias. Entretanto, seu uso tornou-se constante entre os jovens, sendo consumida em festas como um potente alucinó-geno. Já quanto a pesquisas laboratoriais, essa droga tem sido utilizada como modelo para induzir esquizofrenia em animais. Com o objetivo de realizar-se um estudo de revisão da cetamina como anestésico e potencial modelo de esquizofrenia, foi feita uma pesquisa bibliográfica na internet, utilizando programas de pesquisa científica (Pubmed, Medline e Lilacs), além de pesquisa em trabalhos relacionados ao assunto. A administração da cetamina no homem promove o bloqueio dos receptores glutamatérgicos ionotrópicos do tipo N-metil-D-aspartato (NMDA) e antagoniza os receptores de acetilcolina nicotínicos e muscarínicos, bem como os receptores monoaminérgicos e opióides. O bloqueio dos receptores glutamatérgicos promoverá um quadro sintomático semelhante ao de um paciente esquizofrênico. Além disso, a administração da cetamina durante a sinaptogênese pode lesar neurônios corticais, límbicos, talâmicos e estriatais, promovendo uma disfunção na neurotransmissão glutamatérgica e propiciando a manifestação de sintomas psicóticos na vida adulta. Entre esses sintomas, podemos citar o surgimento da esquizofrenia. Somando-se a isso, a droga proporciona uma série de efeitos sistêmicos, desde uma simples anestesia, passando pela sedação, depressão respiratória e até a morte.Palavras-chave: Cetamina, efeitos sistêmicos, esquizofrenia, modelo animal. AbstractKetamine is an anesthetic agent developed in

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Involvement of N-methyl-D-aspartate (NMDA) receptors in noncompetitive NMDA receptor antagonist-induced hyperlocomotion in mice

Cited by 68 publications

References 19 publications

Characteristic Effects of Anti-dementia Drugs on Rat Sleep Patterns

Characteristic Effects of Anti-dementia Drugs on Rat Sleep Patterns

Ketamine, at a Dose that Disrupts Motor Behavior and Latent Inhibition, Enhances Prefrontal Cortex Synaptic Efficacy and Glutamate Release in the Nucleus Accumbens

Cetamina: aspectos gerais e relação com a esquizofrenia

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