Progressive Alterations in Synaptic Transmission and Plasticity of Area CA1 Precede the Cognitive Impairment Associated with Neonatal Administration of MK-801

Hernández-Frausto, Melissa; López‐Rubalcava, Carolina; Galván, Emilio J.

doi:10.1016/j.neuroscience.2019.01.036

Cited by 14 publications

(24 citation statements)

References 69 publications

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“…To elucidate the etiology and pathogenesis of schizophrenia, NMDA receptor antagonists including MK-801 and phencyclidine have been used to induce pharmacological animal models of schizophrenia ( 33 ). Consistent with previous studies that presented schizophrenia-like behaviors in the MK-801 injected animals ( 12 , 13 , 34 ), MK-801 administrated mice demonstrated the increase of locomotor activity, spatial working memory impairment and sensorimotor gating deficit. Quetiapine, an atypical antipsychotic drug, has been widely used in the treatment of schizophrenia and has shown its efficacy in treating positive and negative symptoms, as well as cognitive impairment in schizophrenia patients ( 14 – 16 ).…”

Section: Discussionsupporting

confidence: 91%

“…Our previous study has shown phencyclidine, an NMDA receptor antagonist, induced brain demyelination when administrated in postnatal rats ( 11 ). MK-801, another NMDA receptor antagonist, can cause schizophrenia-like behaviors including prepulse inhibition (PPI) deficit and memory impairment in animals, and is used as a pharmacological model of schizophrenia ( 12 , 13 ).…”

Section: Introductionmentioning

confidence: 99%

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Quetiapine Attenuates Schizophrenia-Like Behaviors and Demyelination in a MK-801–Induced Mouse Model of Schizophrenia

Wen³

et al. 2020

Front. Psychiatry

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Brain demyelination is possibly one of the main pathological factors involved in schizophrenia, and targeting on myelination may be a useful strategy for schizophrenia treatment. Quetiapine, a widely used atypical antipsychotic drug for schizophrenia treatment, has been reported to have neuroprotective effects on cerebral myelination in a demyelination animal model. The objective of the present study was to evaluate the effect and underlying neuroprotective mechanism of quetiapine on the schizophrenia-like behaviors and possible cerebral demyelination induced by MK-801, an N-methyl-Daspartate glutamate receptor antagonist. Mice were treated with chronic quetiapine (10 mg/kg/day, intraperitoneally) for 28 days. From day 22 to 28, 1 h after the administration of quetiapine, the mice were administered MK-801 (2 mg/kg/day, subcutaneously). The positive symptom of schizophrenia was measured in a locomotor activity test on day 29, the memory was evaluated by a Y-maze test on day 30, and the sensorimotor gating deficit in mice was measured by prepulse inhibition test on day 31. After the behavioral tests, the protein expression of myelin basic protein (MBP) was measured by Western Blot, and the protein expression of brain-derived neurotrophic factor (BDNF) was measured by ELISA in the frontal cortex of mice. Our results showed quetiapine attenuated schizophrenia-like behaviors including hyperactivity, memory impairment, and sensorimotor gating deficit in the MK-801 mice. In the same time, quetiapine attenuated demyelination, concurrent with attenuated BDNF decrease in the brain of MK-801-injected mice. These results suggest that the beneficial effects of quetiapine on schizophrenia might be partly related to its neuroprotective effect on brain myelin basic protein and its upregulating neuroprotective proteins such as BDNF, and indicate that modulation of cerebral demyelination could be a novel treatment target of schizophrenia.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Quetiapine Attenuates Schizophrenia-Like Behaviors and Demyelination in a MK-801–Induced Mouse Model of Schizophrenia

Wen³

et al. 2020

Front. Psychiatry

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“…We also offered experimental evidence that pharmacologic activation of dopaminergic transmission via D1 and D5 receptors partially reverts electrophysiologic alterations inflicted by MK‐801. A previous study (Hernández‐Frausto et al, 2019) showed that neonatal treatment with MK‐801 induces early signs of behavioural impairment in young‐adult animals (PND 90) without affecting behaviour in post‐weaning animals (PND 30); another study reported degraded memory performance related to MK‐801 in adult animals (Furuie et al, 2019). Here, by employing a hippocampal‐related memory task, we demonstrate that MK‐801 impairs cognitive performance in young animals.…”

Section: Discussionmentioning

confidence: 99%

Activation of D1/D5 receptors ameliorates decreased intrinsic excitability of hippocampal neurons induced by neonatal blockade of N‐methyl‐d‐aspartate receptors

Griego

Hernández-Frausto

Márquez

et al. 2022

British J Pharmacology

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“…Administration of NMDA antagonists during brain maturation could induce cellular and behavioral alterations that mirror symptoms of schizophrenia [ 1 ]. The deficit of sensorimotor gating affecting the processing of extraneous sensory, cognitive, and motor information is a characteristic symptom of schizophrenia, and sensorimotor gating impairment may be correlative to the cognitive deficits and positive symptoms in schizophrenia [ 9 , 11 , 13 ].…”

Section: Discussionmentioning

confidence: 99%

“…Schizophrenia may be a neurodevelopmental and neurodegenerative disorder, neonatal administration of N -methyl- d -aspartate (NMDA) receptor antagonists such as MK-801 or phencyclidine during brain neurodevelopmental stage induces cerebral neurodegeneration and the symptoms including sensory gating impairment of schizophrenia in rodents [ 1 , 2 ]. Sensory gating can be measured by prepulse inhibition (PPI) which refers to the inhibition of a startle reflex produced by a preceding weak prepulse stimulus [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

Fluoxetine attenuates prepulse inhibition deficit induced by neonatal administration of MK-801 in mice

Yang

Liu²,

Yuan³

et al. 2020

NeuroReport

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Increasing evidence supports schizophrenia may be a neurodevelopmental and neurodegenerative disorder. Fluoxetine, a selective serotonin reuptake inhibitor, has been reported to have neuroprotective effects and be effective in treating neurodegenerative disorders including schizophrenia. The objective of the present study was to evaluate the effect and underlying neuroprotective mechanism of fluoxetine on the sensorimotor gating deficit, a schizophrenia-like behavior in a neurodevelopmental schizophrenic mouse model induced by MK-801, an N -methyl- d -aspartate glutamate receptor antagonist. On postnatal day 7, mouse pups were treated with a total seven subcutaneous daily injections of MK-801 (1 mg/kg/day), followed by intraperitoneal injection of fluoxetine (5 or 10 mg/kg/day) starting on postnatal day 14 in the MK-801-injected mice for 4 weeks. The sensorimotor gating deficit in mice was measured by prepulse inhibition (PPI) behavioral test on postnatal day 43. After the behavioral test, the protein expression of brain-derived neurotrophic factor (BDNF) was measured by western blot or ELISA in the frontal cortex of mice. Our results showed fluoxetine attenuated PPI deficit and the decrease of cerebral BDNF expression in the MK-801-injected mice. These results suggest that fluoxetine can be used to treat sensorimotor gating deficit in a neurodevelopmental mouse model of schizophrenia, and the attenuating effect of fluoxetine on sensorimotor gating deficit may be related to fluoxetine’s neuroprotective effect targeting on the modulation of cerebral BDNF.

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Progressive Alterations in Synaptic Transmission and Plasticity of Area CA1 Precede the Cognitive Impairment Associated with Neonatal Administration of MK-801

Cited by 14 publications

References 69 publications

Quetiapine Attenuates Schizophrenia-Like Behaviors and Demyelination in a MK-801–Induced Mouse Model of Schizophrenia

Quetiapine Attenuates Schizophrenia-Like Behaviors and Demyelination in a MK-801–Induced Mouse Model of Schizophrenia

Activation of D1/D5 receptors ameliorates decreased intrinsic excitability of hippocampal neurons induced by neonatal blockade of N‐methyl‐d‐aspartate receptors

Fluoxetine attenuates prepulse inhibition deficit induced by neonatal administration of MK-801 in mice

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