Microinjection of Reelin into the mPFC prevents MK-801-induced recognition memory impairment in mice

Sawahata, Masahito; Asano, Hiroki; Nagai, Taku; Ito, Norimichi; Kohno, Takao; Nabeshima, Toshitaka; Hattori, Mitsuharu; Yamada, Kiyofumi

doi:10.1016/j.phrs.2021.105832

Cited by 17 publications

(8 citation statements)

References 80 publications

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“…Despite the fact that each author focused on a different region of the brain, most of the alterations were described in the PFC and the hippocampus, being both regions highly involved in SCZ disease. The only three models that overexpress RELN instead of reducing levels are the Teixeira et al (2011) transgenic model, in which they caused this overexpression to study its consequences in mice, the RELN injections models (7 to 9-week-old male mice, Sawahata et al, 2021 ; 6 to 7-week-old male mice, Ishii et al, 2015a ) and the high-fat diet model (12 to 24-week-old mice) ( Roberts et al, 2019 ; Table 5 ). A recent study supports the hypothesis of RELN as a treatment for SCZ.…”

Section: Discussionmentioning

confidence: 99%

Reelin Alterations, Behavioral Phenotypes, and Brain Anomalies in Schizophrenia: A Systematic Review of Insights From Rodent Models

et al. 2022

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Reelin is an extracellular matrix glycoprotein reduced in brain regions (the prefrontal cortex and the hippocampus) of patients with schizophrenia. There are diverse rodent models of schizophrenia that mimic patient symptoms based on various causal theories; however, likely shared reelin alterations have not yet been systematically assessed in those models. A systematic review of the literature was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) model. Articles focused on psychotic disorders or schizophrenia and their relationship with reelin in rodent models were selected. Data (first author, publication year, results, both open field and prepulse inhibition test results, and type of reelin alteration) were extracted in duplicate by two independent reviewers. The 37 reviewed articles reported about various schizophrenia models and their reelin alterations, brain morphology, and behavioral defects. We conclude that reelin is an altered preclinical biomarker common to all models included, mainly prenatal or genetic models, and a key protein in schizophrenia disease, making the reelin signaling pathway in prenatal stages a target of special interest for future preclinical and clinical studies. All models presented at least one of the four described reelin alteration types.Systematic Review Registration: [https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42021210568], identifier [CRD42021210568].

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Section: Discussionmentioning

confidence: 99%

Reelin Alterations, Behavioral Phenotypes, and Brain Anomalies in Schizophrenia: A Systematic Review of Insights From Rodent Models

et al. 2022

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“…On the contrary, the long-term continuous stress (over 4 weeks) greatly reduced the expression of Reelin protein in the hippocampus, along with the chronic-stress-induced downregulation of the syn-PSD-95 protein in the synapses. Therefore, it indicated that decreased expression of Reelin and aggregation of PSD-95 protein in the synapses may be linked to one of the mechanisms underlying the transition from adaptation to pathology [ 19 , 20 , 58 , 59 , 60 ].…”

Section: Discussionmentioning

confidence: 99%

A Moderate Duration of Stress Promotes Behavioral Adaptation and Spatial Memory in Young C57BL/6J Mice

et al. 2022

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Stress may serve multiple roles in cerebral functioning, ranging from a highly appropriate behavioral adaptation to a critical risk factor for susceptibility to mood disorder and cognitive impairment. It is well known that E/I (excitation/inhibition) balance is essential for maintaining brain homeostasis. However, it remains largely unknown how GABAergic and Glutamatergic neurons respond to different stressful stimuli and whether the GABAergic-Glutamatergic neuron balance is related to the transition between adaptive and maladaptive behaviors. Here, we subjected 3-month-old mice to chronic mild stress (CMS) for a period of one, two, and four weeks, respectively. The results showed that the two-week CMS procedure produced adaptive effects on behaviors and cognitive performance, with a higher number of GABAergic neuron and VGluT1-positive neurons, increasing the expressions of p-GluN2B, Reelin, and syn-PSD-95 protein in the hippocampus. In contrast, the prolonged behavioral challenge (4 week) imposes a passive coping behavioral strategy and cognitive impairment, decreased the number of GABAergic neuron, hyperactivity of VGluT1-positive neuron, increased the ratio of p-GluN2B, and decreased the expression of Reelin, syn-PSD-95 in the hippocampus. These findings suggest that a moderate duration of stress probably promotes behavioral adaptation and spatial memory by maintaining a GABAergic-Glutamatergic neuron balance and promoting the expression of synaptic plasticity-related proteins in the brain.

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“…It also increases glucose metabolism and induces heat shock protein and necrotic cell death in neurons [70 , 71] . Glutamate transmission has a significant role in behavioural systems such as motor activity, learning, and cognition [73 , 74] . MK-801 also alters dopamine levels in the prefrontal cortex, resulting in motor dysfunction [73] .…”

Section: Methods Detailsmentioning

confidence: 99%

Experimentally induced animal models for cognitive dysfunction and Alzheimer's disease

2022

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Microinjection of Reelin into the mPFC prevents MK-801-induced recognition memory impairment in mice

Cited by 17 publications

References 80 publications

Reelin Alterations, Behavioral Phenotypes, and Brain Anomalies in Schizophrenia: A Systematic Review of Insights From Rodent Models

Reelin Alterations, Behavioral Phenotypes, and Brain Anomalies in Schizophrenia: A Systematic Review of Insights From Rodent Models

A Moderate Duration of Stress Promotes Behavioral Adaptation and Spatial Memory in Young C57BL/6J Mice

Experimentally induced animal models for cognitive dysfunction and Alzheimer's disease

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