NOGO-66 receptor deficient mice show slow acquisition of spatial memory task performance

Gaalen, Marcel M. van; Relo, Ana Lucia; Mueller, Bernhard K.; Groß, Gerhard; Mezler, Mario

doi:10.1016/j.neulet.2012.01.004

Cited by 20 publications

(13 citation statements)

References 18 publications

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“…The known involvement of the receptor protein in modulation of axonal outgrowth (Cafferty and Strittmatter 2006; Cafferty, W.B. 2006) and plasticity (McGee et al 2005) is consistent with animal models that have shown decreased spatial learning and memory function as a result of reduced expression (van Gaalen et al 2012). As this gene lies within the 22q11 locus, and is associated with myelin-mediated inhibition of axonal sprouting (Budel et al 2008), our data suggest that altered dosage of this gene (by virtue of the presence of only one copy this gene in individuals with 22q11.2DS) may underlie alterations in the white matter tracts of individuals with this syndrome.…”

Section: Discussionsupporting

confidence: 72%

White matter abnormalities in 22q11.2 deletion syndrome: Preliminary associations with the Nogo-66 receptor gene and symptoms of psychosis

Perlstein

Chohan

Coman

et al. 2014

Schizophrenia Research

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Background This study utilized diffusion tensor imaging (DTI) to analyze white matter tractography in anterior limb of the internal capsule (ALIC), fornix, and uncinate fasciculus (UF) of individuals with 22q11.2 Deletion Syndrome and controls. Aberrations in these tracts have been previously associated with schizophrenia. With up to 25% of individuals with 22q11.2DS developing schizophrenia in adulthood, we hypothesized reduction in structural integrity of these tracts, including an association with prodromal symptoms of psychosis. We further predicted association between allelic variation in a functional polymorphism of the NoGo-66 receptor gene and 22q11.2DS white matter integrity. Methods Tractography was conducted using fiber assignment by streamline tracking algorithm in DTI studio. Subjects were genotyped for the rs701428 SNP of the Nogo-66 receptor gene, and assessed for presence of prodromal symptoms. Results We found significant group differences between 22q11.2DS and controls in DTI metrics for all three tracts. DTI metrics of ALIC and UF were associated with prodromal symptoms in 22q11.2DS. Further, ALIC DTI metrics were associated with allelic variation of the rs701428 SNP of the NoGo-66 receptor gene in 22q11.2DS. Conclusions Alterations in DTI metrics suggest white matter microstructural anomalies of the ALIC, fornix, and UF in 22q11.2DS. Structural differences in ALIC appear to be associated with the Nogo-66 receptor gene, which has been linked to myelin-mediated axonal growth inhibition. Moreover, the association between psychosis symptoms and ALIC and UF metrics suggests that the Nogo-66 receptor gene may represent a susceptibility gene for psychosis through its disruption of white matter microstructure and myelin-associated axonal growth.

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Section: Discussionsupporting

confidence: 72%

White matter abnormalities in 22q11.2 deletion syndrome: Preliminary associations with the Nogo-66 receptor gene and symptoms of psychosis

Perlstein

Chohan

Coman

et al. 2014

Schizophrenia Research

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“…Its gene is located within 22q11.2 segment A. Budel et al () argued that its variants with a loss‐of‐function may alter neuronal growth and myelinization; they also found a reduced working memory in mice lacking this gene. Furthermore, RTN4R(−/−) mice have proven to have deficits in spatial learning (Lazar et al, ) and memory task (van Gaalen, Relo, Mueller, Gross, & Mezler, ). Thompson et al () found a correlation between a specific allelic variation of this gene and reduced posterior cerebral volumes, which are thought to be responsible for some visual and social cognitive deficits of the syndrome.…”

Section: Social Cognition Relationships With Specific Phenotypes Of 2mentioning

confidence: 99%

Genetic and clinical features of social cognition in 22q11.2 deletion syndrome

Lattanzi

Buzzanca

Frascarelli

et al. 2018

J of Neuroscience Research

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22q11.2 deletion syndrome (22q11.2 DS) is widely known as one of the most compelling genetic models of schizophrenia so far, being almost 40% of the carriers affected by psychotic symptoms. Moreover, most of these subjects also show impairment in social cognition, which is a comprehensive array of function that guides social interaction with the others, leading as well to the acquisition of new cognitive and social skills. In the last decade researchers have argued whether social cognition dysfunctions could be underlined by specific genetic alterations, and whether these are linked to specific clinical features. Some valid candidate genes are RTN4R, that encodes a protein which inhibits axonal sprouting, DGCR8, crucial in mRNA processing, or catechol-O-methyltransferase (COMT) and proline oxydase 1 (PRODH), involved in catecholamine metabolism in frontal cortex. This is the first article to address the topic of social cognition in 22q11.2 DS from a wide perspective, with a highlight on its genetic characteristics. We will provide a narrative review of the most recent findings and we will point out new directions on this research path, in order to achieve an effective characterization of the neurobiological system underlying social behavior.

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“…Recent evidence suggests that interfering with growth inhibitory signaling cascades may have detrimental consequences for intellectual abilities by impairing key neurologic functions such as long-term memory storage and mental health. Loss of NgR1 does not impair hippocampal learning in the Morris Water Maze (MWM), and forebrain-specific overexpression of NgR1 does not alter short-term memory [97, 98]; however, it does impair the formation of long-lasting memory in the MWM task [98]. In the amygdala, ChaseABC digestion of CS-GAGs renders acquired fear memory susceptible to erasure, supporting the notion that stable synapses are important for long-term memory storage [99].…”

Section: Are Some Things Not Meant To Be Undone?mentioning

confidence: 99%

Where no synapses go: gatekeepers of circuit remodeling and synaptic strength

Mironova

Giger

2013

Trends in Neurosciences

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Growth inhibitory molecules in the adult mammalian CNS have been implicated in blocking axonal sprouting and regeneration following injury. Prominent CNS regeneration inhibitors include Nogo-A, OMgp and CSPGs, and a key question concerns their physiological role in the naïve CNS. Emerging evidence suggests novel functions in dendrites and at synapses of glutamatergic neurons. CNS regeneration inhibitors target the neuronal actin cytoskeleton to regulate dendritic spine maturation, long-term synapse stability, and Hebbian forms of synaptic plasticity. This is accomplished in part by antagonizing plasticity-promoting signaling pathways activated by neurotrophic factors. Altered function of CNS regeneration inhibitors is associated with mental illness and loss of long-lasting memory, suggesting unexpected and novel physiological roles for these molecules in brain health.

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NOGO-66 receptor deficient mice show slow acquisition of spatial memory task performance

Cited by 20 publications

References 18 publications

White matter abnormalities in 22q11.2 deletion syndrome: Preliminary associations with the Nogo-66 receptor gene and symptoms of psychosis

White matter abnormalities in 22q11.2 deletion syndrome: Preliminary associations with the Nogo-66 receptor gene and symptoms of psychosis

Genetic and clinical features of social cognition in 22q11.2 deletion syndrome

Where no synapses go: gatekeepers of circuit remodeling and synaptic strength

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