Genetic Analysis of Synaptogenesis

Lu, Cecilia S.; Vactor, David Van

doi:10.1016/b978-0-12-397266-8.00104-6

Cited by 3 publications

(2 citation statements)

References 470 publications

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“…Given that spines are the site for neurons to receive synaptic transmission, changes in spine morphology and numbers can be a fundamental indicator of physiological or pathological changes in the brain (Berry and Nedivi, 2017;Herms and Dorostkar, 2016;Moser et al, 1994;Perez-Cruz et al, 2011). The molecular mechanisms that regulate spine genesis (synaptogenesis) and removal (synaptic pruning) have been intensively studied (Kilinc, 2018;Lu and Van Vactor, 2013;Sudhof, 2018). Accumulating evidence has revealed that components of the complement system (C1q, C3, and C4) and microglia play important roles in regulation of synaptic refinement and elimination during developmental synaptogenesis in the CNS (Mastellos, 2014;Presumey et al, 2017;Schafer et al, 2012;Tenner et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

The Complement Regulator Susd4 Influences Nervous-System Function and Neuronal Morphology in Mice

et al. 2020

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The SUSD4 (Sushi domain-containing protein 4) gene encodes a complement inhibitor that is frequently deleted in 1q41q42 microdeletion syndrome, a multisystem congenital disorder that includes neurodevelopmental abnormalities. To understand SUSD4's role in the mammalian nervous system, we analyzed Susd4 knockout (KO) mice. Susd4 KO mice exhibited significant defects in motor performance and significantly higher levels of anxiety-like behaviors. Susd4 KO brain had abnormal ''hairy'' basket cells surrounding Purkinje neurons within the cerebellum and significantly reduced dendritic spine density in hippocampal pyramidal neurons. Neurons and oligodendrocyte lineage cells of wild-type mice were found to express Susd4 mRNA. Protein expression of the complement component C1q was increased in the brains of Susd4 KO mice. Our data indicate that SUSD4 plays an important role in neuronal functions, possibly via the complement pathway, and that SUSD4 deletion may contribute to the nervous system abnormalities in patients with 1q41q42 deletions.

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Section: Discussionmentioning

confidence: 99%

The Complement Regulator Susd4 Influences Nervous-System Function and Neuronal Morphology in Mice

et al. 2020

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“…In the synaptic cleft, they bind and activate neurotransmitter receptors within the postsynaptic membrane. [ 2 23 35 54 55 ] In fact, the most principal function in the presynaptic buttons is the regulated release of neurotransmitter in a tightly regulated process called exocytosis which is accomplished through the fusions of synaptic vesicles with the presynaptic membrane. [ 23 54 56 ] Several lines of studies were carried out to characterize the components of the synaptic vesicle membrane and found a number of proteins, including SYP, synaptotagmin, and synaptobrevin that functions as the regulators of exocytosis.…”

Section: Discussionmentioning

confidence: 99%

Synaptogenesis in the cerebellum of offspring born to diabetic mothers

et al. 2017

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There is increasing evidence that maternal diabetes mellitus during the pregnancy is associated with a higher risk of neurodevelopmental and neurofunctional anomalies including motor dysfunctions, learning deficits, and behavioral problems in offspring. The cerebellum is a part of the brain that has long been recognized as a center of movement balance and motor coordination. Moreover, recent studies in humans and animals have also implicated the cerebellum in cognitive processing, sensory discrimination, attention, and learning and memory. Synaptogenesis is one of the most crucial events during the development of the central nervous system. Synaptophysin (SYP) is an integral membrane protein of synaptic vesicles and is considered to be a marker for synaptic density and synaptogenesis. Here, we review the manuscripts focusing on the negative impacts of maternal diabetes in pregnancy on the expression or localization of SYP in the developing cerebellar cortex. We believe that the alteration in synaptogenesis or synapse density may be part of the cascade of events through which diabetes in pregnant women affects the newborn's cerebellum.

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Altered expression and localization of synaptophysin in developing cerebellar cortex of neonatal rats due to maternal diabetes mellitus

et al. 2016

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There is sufficient evidence that diabetes during pregnancy is associated with a higher risk of neurodevelopmental anomalies including learning deficits, behavioral problems and motor dysfunctions in the offspring. Synaptophysin (SYP) is an integral membrane protein of synaptic vesicles and is considered as a marker for synaptogenesis and synaptic density. This study aimed to examine the effects of maternal diabetes in pregnancy on the expression and localization of SYP in the developing rat cerebellum. Wistar female rats were maintained diabetic from a week before pregnancy through parturition and male offspring was euthanized at postnatal day (P) 0, 7, and 14. The results revealed a significant down-regulation in the mRNA expression of SYP in the offspring born to diabetic animals at both P7 and P14 (P < 0.05 each). One week after birth, there was a significant reduction in the localization of SYP expression in the external granular (EGL) and in the molecular (ML) layers of neonates born to diabetic animals (P < 0.05 each). We also found a marked decrease in the expression of SYP in all of the cerebellar cortical layers of STZ-D group pups at P14 (P < 0.05 each). Moreover, our results revealed no significant changes in either expression or localization of SYP in insulin-treated group pups when compared with the controls (P ≥ 0.05 each). The present study demonstrated that maternal diabetes has adverse effects on the synaptogenesis in the offspring's cerebellum. Furthermore, the rigid maternal blood glucose control in the most cases normalized these negative impacts.

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Genetic Analysis of Synaptogenesis

Cited by 3 publications

References 470 publications

The Complement Regulator Susd4 Influences Nervous-System Function and Neuronal Morphology in Mice

The Complement Regulator Susd4 Influences Nervous-System Function and Neuronal Morphology in Mice

Synaptogenesis in the cerebellum of offspring born to diabetic mothers

Altered expression and localization of synaptophysin in developing cerebellar cortex of neonatal rats due to maternal diabetes mellitus

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