N-Cadherin Regulates GluA1-Mediated Depressive-Like Behavior in Adolescent Female Rat Offspring following Prenatal Stress

Shao, Shuya; Yao, Dan; Li, Senya; Li, Jing; Si, Yufang; Zhang, Huiping; Zhu, Zhongliang; Song, Dongli; Li, Hui

doi:10.1159/000518383

Cited by 4 publications

(3 citation statements)

References 53 publications

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“…59,60 Conversely, increased SYN 1 and PSD 95 expression can improve depression. 61,62 Consistent with our findings, GRd greatly reversed the significant decrease in SYN 1 and PSD 95 protein levels in the hippocampus of CUMS rats. This shows that the antidepressant-like effect of GRd is linked to the expression of hippocampal synaptic plasticity-related regulators.…”

Section: Discussionsupporting

confidence: 90%

Antidepressant-Like Effect and Mechanism of Ginsenoside Rd on Rodent Models of Depression

Wang

Zhang

et al. 2022

DDDT

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Background: There is growing evidence to suggest that ginsenoside Rd (GRd) has a therapeutic effect on depression, but the specific mechanisms behind its activity require further study. Objective: This study is designed to investigate the antidepressant-like effect and underlying mechanisms of GRd. Methods: In this study, the behavioral despair mouse model of depression and chronic unpredictable mild stress (CUMS) rat model of depression were established to explore the effects of GRd on depression-like behavior and its underlying mechanisms. Behavioral tests were used to evaluate the replication of animal models and depression-like behaviors. The hypoxia-inducible factor-1α (HIF-1α) blocker 2-methoxyestradiol (2-ME) was injected to determine the role of HIF-1α in the antidepressant-like effect of GRd. In addition, molecular biology techniques were used to determine the mRNA and protein expression of HIF-1ɑ signaling pathway and synaptic plasticity-related regulators, that is synapsin 1 (SYN 1) and postsynaptic density protein 95 (PSD 95). In silico binding interaction studies of GRd with focused target proteins were performed using molecular docking to predict the affinity and optimal binding mode between ligands and receptors. Results: Our data show that GRd significantly reversed depression-like behavior and promoted mRNA and protein expression of HIF-1ɑ signaling pathway and synaptic plasticity-related regulators. However, the antidepressant-like effect of GRd disappeared upon inhibition of HIF-1α expression following administration of 2-ME. Furthermore, molecular docking results showed that GRd possessed significant binding affinity for HIF-1α, VEGF, and VEGFR-2. Conclusion: Our results show that GRd exhibits significant antidepressant-like effect and that HIF-1α signaling pathway is a promising target for the treatment of depression.

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Section: Discussionsupporting

confidence: 90%

Antidepressant-Like Effect and Mechanism of Ginsenoside Rd on Rodent Models of Depression

Wang

Zhang

et al. 2022

DDDT

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“…GluA1 is critical for LTP and is associated with several neurological diseases (Ge & Wang, 2021; Gugustea & Jia, 2021). Based on genome‐wide association studies (GWAS), GluA1 dysfunction has been identified as a risk factor for schizophrenia (Ripke et al., 2014), while molecular and pharmacological studies in the last decade have identified GluA1 in depression, anxiety, stress‐related behavior and Alzheimer's disease (Minano‐Molina et al., 2011; Shao et al., 2021). Interestingly, GluA1 expression and phosphorylation levels appear to be important for these neurological conditions (An et al., 2021; Leal et al., 2020; Minano‐Molina et al., 2011; Roman‐Albasini et al., 2020).…”

Section: Discussionmentioning

confidence: 99%

Gender‐related variation expressions of neuroplastin TRAF6, GluA1, GABA(A) receptor, and PMCA in cortex, hippocampus, and brainstem in an experimental epilepsy model

Doğanyiğit,

Okan,

Yılmaz

et al. 2024

Synapse

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Epileptic seizures are seen as a result of changing excitability balance depending on the deterioration in synaptic plasticity in the brain. Neuroplastin, and its related molecules which are known to play a role in synaptic plasticity, neurotransmitter activities that provide balance of excitability and, different neurological diseases, have not been studied before in epilepsy.In this study, a total of 34 Sprague–Dawley male and female rats, 2 months old, weighing 250–300 g were used. The epilepsy model in rats was made via pentylenetetrazole (PTZ). After the completion of the experimental procedure, the brain tissue of the rats were taken and the histopathological changes in the hippocampus and cortex parts and the brain stem were investigated, as well as the immunoreactivity of the proteins related to the immunohistochemical methods.As a result of the histopathological evaluation, it was determined that neuron degeneration and the number of dilated blood vessels in the hippocampus, frontal cortex, and brain stem were higher in the PTZ status epilepticus (SE) groups than in the control groups. It was observed that neuroplastin and related proteins TNF receptor‐associated factor 6 (TRAF6), Gamma amino butyric acid type A receptors [(GABA(A)], and plasma membrane Ca2+ ATPase (PMCA) protein immunoreactivity levels increased especially in the male hippocampus, and only AMPA receptor subunit type 1 (GluA1) immunoreactivity decreased, unlike other proteins.We believe this may be caused by a problem in the mechanisms regulating the interaction of neuroplastin and GluA1 and may cause problems in synaptic plasticity in the experimental epilepsy model. It may be useful to elucidate this mechanism and target GluA1 when determining treatment strategies.

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“…In GluA1-deficient mice, hippocampal LTP was absent without spatial reference memory deficits [67], but working memory deficits [68], schizophrenia-like behaviors [69,70] and increased locomotor activity, accompanied by reduced clearance of striatal dopamine, was displayed [69]. While GWAS identified GluA1 dysfunction as a risk factor for schizophrenia [12], molecular and pharmacological studies over the past decade have linked GluA1 to depression, anxiety, stress-related behavior, and Alzheimer's disease [71][72][73][74]. Interestingly, the levels of GluA1 expression and phosphorylation appear to be important for these neurological conditions [71,73,75,76].…”

Section: Figurementioning

confidence: 99%

Neuroplastin in Neuropsychiatric Diseases

Lin

Liang

Herrera-Molina

et al. 2021

Genes

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Molecular mechanisms underlying neuropsychiatric and neurodegenerative diseases are insufficiently elucidated. A detailed understanding of these mechanisms may help to further improve medical intervention. Recently, intellectual abilities, creativity, and amnesia have been associated with neuroplastin, a cell recognition glycoprotein of the immunoglobulin superfamily that participates in synapse formation and function and calcium signaling. Data from animal models suggest a role for neuroplastin in pathways affected in neuropsychiatric and neurodegenerative diseases. Neuroplastin loss or disruption of molecular pathways related to neuronal processes has been linked to various neurological diseases, including dementia, schizophrenia, and Alzheimer’s disease. Here, we review the molecular features of the cell recognition molecule neuroplastin, and its binding partners, which are related to neurological processes and involved in learning and memory. The emerging functions of neuroplastin may have implications for the treatment of diseases, particularly those of the nervous system.

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N-Cadherin Regulates GluA1-Mediated Depressive-Like Behavior in Adolescent Female Rat Offspring following Prenatal Stress

Cited by 4 publications

References 53 publications

Antidepressant-Like Effect and Mechanism of Ginsenoside Rd on Rodent Models of Depression

Antidepressant-Like Effect and Mechanism of Ginsenoside Rd on Rodent Models of Depression

Gender‐related variation expressions of neuroplastin TRAF6, GluA1, GABA(A) receptor, and PMCA in cortex, hippocampus, and brainstem in an experimental epilepsy model

Neuroplastin in Neuropsychiatric Diseases

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