Differential expression of synaptic markers regulated during neurodevelopment in a rat model of schizophrenia-like behavior

Elfving, Betina; Müller, Heidi Kaastrup; Oliveras, Ignasi; Østerbøg, Tina Becher; Río-Álamos, Cristóbal; Sánchez-González, Ana; Tobeña, Adolf; Fernandez-Teruel, Alberto; Aznar, Susana

doi:10.1016/j.pnpbp.2019.109669

Cited by 35 publications

(19 citation statements)

References 86 publications

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“…This may indicate that dysfunction of NMDA receptor subunits can serve as a trigger for the development of schizophrenia, and significant mutations in the GRIN2A and GRIN2B genes can affect early or late onset. Studies in rat models have shown that GRIN2A and GRIN2B expression is upregulated in the prefrontal cortex during childhood and adolescence, while a model of schizophrenia is characterized by an immature neurobiological phenotype with reduced GRIN2A and GRIN2B expression [36]. This suggests the importance of the age at which dysfunction of the NMDA receptor subunits triggers the pathological defect.…”

Section: Discussionmentioning

confidence: 99%

Study of Early Onset Schizophrenia: Associations of GRIN2A and GRIN2B Polymorphisms

Poltavskaya

Fedorenko

Kornetova

et al. 2021

Life

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Background: Schizophrenia is a complex mental disorder with a high heritability. Dysfunction of the N-methyl-D-aspartate (NMDA)-type glutamate receptors may be involved in the pathogenesis of schizophrenia. In this study, we examined the contribution of GRIN2A and GRIN2B (Glutamate Ionotropic Receptor NMDA Type Subunit 2A/2B) polymorphisms to the clinical features of schizophrenia, such as the leading symptoms, the type of course, and the age of onset. Methods: A population of 402 Russian patients with schizophrenia from the Siberian region was investigated. Genotyping of seventeen single-nucleotide polymorphisms (SNPs) in GRIN2A and GRIN2B was performed using QuantStudio™ 3D Digital PCR System Life Technologies amplifier using TaqMan Validated SNP Genotyping Assay kits (Applied Biosystems). The results were analyzed using Chi-square and the Fisher’s exact tests. Results: We found an association of GRIN2A rs7206256 and rs11644461 and GRIN2B rs7313149 with the early onset (before the age of 18 years old) schizophrenia. We did not reveal any associations of GRIN2A and GRIN2B polymorphisms with leading (positive vs. negative) symptoms or type of course (continuous vs. episodic) of schizophrenia. Conclusions: In the study, we confirmed the involvement of the GRIN2A and GRIN2B genes in the early onset of schizophrenia in a Russian population of the Siberian region.

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Section: Discussionmentioning

confidence: 99%

Study of Early Onset Schizophrenia: Associations of GRIN2A and GRIN2B Polymorphisms

Poltavskaya

Fedorenko

Kornetova

et al. 2021

Life

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“…Studies have shown that in inbred Roman High-Avoidance (RHA-I) strain rats with poor learning and memory ability and cognitive impairment, some synaptic-related molecules show different trends in hippocampus and prefrontal cortex. 45 Of course, whether there are also molecular pathways related to cognitive impairment caused by trigeminal neuralgia in prefrontal cortex can be the direction of our future research.…”

Section: Discussionmentioning

confidence: 99%

Trigeminal neuralgia causes neurodegeneration in rats associated with upregulation of the CD95/CD95L pathway

et al. 2020

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Objectives: To explore the effects of trigeminal neuralgia on neurodegeneration in rats and the underlining mechanism. Methods: Sixty adult male Sprague Dawley rats were divided randomly into Chronic Constriction Injury of the Rat's Infraorbital Nerve (ION-CCI) group and sham group (n ¼ 30). Right suborbital nerve was ligated in ION-CCI group to establish a trigeminal neuralgia model. In sham group, suborbital nerve was exposed without ligation. Pain thresholds were measured before surgery and 1, 7, 15, and 30 days after surgery (n ¼ 10). Morris water maze tests (n ¼ 10) were conducted at 1, 15, and 30 days after surgery to evaluate the changes in learning and memory ability of rats. At 5, 19, and 34 days after surgery, serum S100b protein concentration and hippocampal Ab1-42 protein expression were detected by enzyme-linked immunosorbent assay; total tau protein expression was detected by Western blotting; changes of neurons in hippocampus were observed by Nissl staining; and the expression of ser404 p-tau, cluster of differentiation (CD)95, CD95L, and cleaved caspase-3 proteins was detected by immunofluorescence and Western blotting. Results: Hyperalgesia occurred in ION-CCI group, and mechanical pain threshold decreased significantly (P < 0.05). On the 15th and 30th days after surgery, ION-CCI group showed lower learning and memory ability than sham group (P < 0.05). Serum S100b protein concentration, hippocampal A b1-42, and ser404 p-tau protein expression increased in the ION-CCI group 19 and 34 days after surgery (P < 0.05), hippocampal CD95 expression increased in the ION-CCI group after surgery (P < 0.05), hippocampal CD95L expression increased at 19 and 34 days after surgery (P < 0.05), and cleaved caspase-3 expression increased at 5 and 19 days after surgery (P < 0.05). Nissl bodies in ION-CCI group decreased significantly at 15 days after surgery. The expression of cleaved caspase-3 protein in ION-CCI group was positively correlated with the expression of CD95 and CD95L (P < 0.05). Conclusions: Trigeminal neuralgia may lead to neuronal inflammation and neuronal apoptosis associated with upregulation of CD95/CD95L expression, thus causing neurodegeneration.

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“…It is known that the synaptosomal-associated protein 25 (SNAP25), together with syntaxin-1A (STX1A) and vesicle-associated membrane protein 2 (VAMP2), mediates neurotransmitters released by the fusion of synaptic vesicles [162,163]. It was also already reported that alterations in gene expression of SNAP25 in mammals are associated with schizophrenia-like behavior [164], and sequence variations in the SNAP25 locus are associated with attention-deficit/hyperactivity disorder (ADHD) [165][166][167].…”

Section: Synaptic Vesicle Trafficking and Exocytosismentioning

confidence: 99%

Non-Syndromic Intellectual Disability and Its Pathways: A Long Noncoding RNA Perspective

Barros

Leão

Santis

et al. 2021

ncRNA

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Non-syndromic intellectual disability (NS-ID or idiopathic) is a complex neurodevelopmental disorder that represents a global health issue. Although many efforts have been made to characterize it and distinguish it from syndromic intellectual disability (S-ID), the highly heterogeneous aspect of this disorder makes it difficult to understand its etiology. Long noncoding RNAs (lncRNAs) comprise a large group of transcripts that can act through various mechanisms and be involved in important neurodevelopmental processes. In this sense, comprehending the roles they play in this intricate context is a valuable way of getting new insights about how NS-ID can arise and develop. In this review, we attempt to bring together knowledge available in the literature about lncRNAs involved with molecular and cellular pathways already described in intellectual disability and neural function, to better understand their relevance in NS-ID and the regulatory complexity of this disorder.

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Differential expression of synaptic markers regulated during neurodevelopment in a rat model of schizophrenia-like behavior

Cited by 35 publications

References 86 publications

Study of Early Onset Schizophrenia: Associations of GRIN2A and GRIN2B Polymorphisms

Study of Early Onset Schizophrenia: Associations of GRIN2A and GRIN2B Polymorphisms

Trigeminal neuralgia causes neurodegeneration in rats associated with upregulation of the CD95/CD95L pathway

Non-Syndromic Intellectual Disability and Its Pathways: A Long Noncoding RNA Perspective

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