Tyrosine phosphorylation of synaptophysin in synaptic vesicle recycling

Evans, Gareth J.; Cousin, Michael A.

doi:10.1042/bst0331350

Cited by 70 publications

(39 citation statements)

References 51 publications

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“…Its role in the synaptic vesicle life cycle is still relatively unknown, although it is now almost universally agreed that it may have a role in determining synaptic strength (Evans and Cousin, 2005). In the present study, the expression of synaptophysin was increased in the frontal cortex and hippocampus of rats prenatally exposed to LPS, at the age of 6 months, in the absence of changes in GAP-43.…”

Section: Prenatal Lps Exposure Enhances Expression Of Synaptophysin Isupporting

confidence: 48%

Neurobehavioral and Immunological Consequences of Prenatal Immune Activation in Rats. Influence of Antipsychotics

Romero

Ali

Molina‐Holgado

et al. 2006

Neuropsychopharmacol

129

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Increasing evidence suggests that pre-or perinatal events that influence the immune system contribute to the development of behavioral or neuropsychiatric disorders. For instance, exposure of pregnant rats to the bacterial endotoxin lipopolysaccharide (LPS) disrupts sensorimotor information processing, as assessed by the prepulse inhibition test (PPI), and also the immune function in adult offspring, which might be of particular relevance as regards schizophrenia. However, the consequences of maternal LPS exposure during pregnancy on synaptic functioning in adult offspring and, more importantly, the therapeutic opportunity to re-establish PPI and immune function have still to be demonstrated. In this work, we analyzed the consequences of prenatal LPS exposure on dopaminergic neurotransmission and presynaptic markers in adult brain areas related to PPI circuitry. In addition, we tested whether oral treatment with the typical antipsychotic drug haloperidol (HAL) could reinstate PPI performances and cytokine serum levels in six-month-old male rats with prenatal LPS exposure. Both sensory information processing deficits and immune anomalies induced by prenatal exposure to LPS were accompanied by changes in dopaminergic neurotransmission and synaptophysin expression. It is important to note that PPI disruption and serum increases in cytokines induced by prenatal LPS exposure were both reversed by HAL. Taken together, these results demonstrate the critical influence of prenatal immune events on the functioning of adult nervous and immune systems, in association with the putative role of the immune system in the development of behavior relevant to schizophrenia.

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Section: Prenatal Lps Exposure Enhances Expression Of Synaptophysin Isupporting

confidence: 48%

Neurobehavioral and Immunological Consequences of Prenatal Immune Activation in Rats. Influence of Antipsychotics

Romero

Ali

Molina‐Holgado

et al. 2006

Neuropsychopharmacol

129

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“…In addition, synaptophysin levels have been shown to correlate with resting-state brain glucose utilization (Rocher et al 2003). The function of this protein is still unknown but previous suggestions have included calcium binding (Rehm et al 1986), channel formation (Sudhof et al 1987;Thomas et al 1988), exocytosis (Alder et al 1992Mullany and Lynch 1998), and synaptic vesicle recycling via endocytosis (Evans and Cousin 2005). Furthermore, synaptophysin has also been implicated in disorders of neurodevelopment such as schizophrenia.…”

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confidence: 99%

Synaptophysin and postsynaptic density protein 95 in the human prefrontal cortex from mid-gestation into early adulthood

Glantz¹,

Gilmore²,

Hamer³

et al. 2007

Neuroscience

234

162

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Previous studies of postnatal synaptic development in human frontal cortex have shown that synaptic density rises after birth, reaches a plateau in childhood and then decreases to adult levels by late adolescence. A similar pattern has been seen in nonhuman primate cortex. These earlier studies in human cortex are limited, however, by significant age gaps in study subjects at critical inflection points of the developmental curve. Additionally, it is unclear if synaptic development occurs in different patterns in different cortical layers in prefrontal cortex (PFC). The purpose of this study was to examine synaptic density in human PFC across development by measuring two synaptic marker proteins: synaptophysin (presynaptic), and postsynaptic density-95 (PSD-95; postsynaptic). Western blotting was used to assess the relative levels of synaptophysin and PSD-95 in dorsolateral PFC of 42 subjects, distributed in age from 18 weeks gestation to 25 years. In addition, synaptophysin immunoreactivity was examined in each layer of areas 9 and 46 of PFC in 24 subjects, ranging in age from 0.1 to 25 years. Synaptophysin levels slowly increased from birth until age 5 and then increased more rapidly to peak in late childhood around age 10. Synaptophysin subsequently decreased until the adult level was reached by mid-adolescence, around age 16. PSD-95 levels increased postnatally to reach a stable plateau by early childhood with a slight reduction in late adolescence and early adulthood. The pattern of synaptophysin immunoreactivity seen with immunohistochemistry was similar to the Western experiments but the changes across age were more subtle, with little change by layer within and across age. The developmental patterns exhibited by these synaptic marker proteins expand upon previous studies of developmental synaptic changes in human frontal cortex; synaptic density increases steadily from birth to late childhood, then decreases in early adolescence to reach adult levels by late adolescence. Keywordsadolescence; development; human; synapses; pruning; synaptogenesisThe human brain has the most protracted period of development of any species, with neurodevelopment continuing well into early adulthood. Imaging studies have shown that in the human, the overall volume of the brain increases during childhood and adolescence (Giedd Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2008 November 9. Sowell et al. 2002;Gilmore et al. 2007). Specifically, the cortical gray matter volume, particularly the f...

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“…Intact information transfer is seemingly crucial for learning and memory, therefore the maintenance of neurotransmission is partially dependent on synaptic vesicle endocytosis and recycling. Synaptophysin is involved, although unclear how, in regulating the life cycle of synaptic vesicles, and that its function is controlled by phosphorylation (Evans and Cousin, 2005).…”

Section: Discussionmentioning

confidence: 99%

A single neonatal exposure to perfluorohexane sulfonate (PFHxS) affects the levels of important neuroproteins in the developing mouse brain

Lee

Viberg

2013

NeuroToxicology

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A single neonatal exposure to perfluorohexane sulfonate (PFHxS) affects the levels of important neuroproteins in the developing mouse brain. , 37: 190-196 Neurotoxicology AbstractPerfluorohexane sulfonate (PFHxS) is an industrial chemical and belongs to the group of perfluorinated compounds (PFCs). It has recently been shown to cause developmental neurobehavioral defects in mammals. These compounds are commonly used in products such as surfactant and protective coating due to their ability to repel water-and oil stains. PFCs are globally found in the environment as well as in human umbilical cord blood, serum and breast milk. In a previous study on other well-known PFCs i.e. PFOS and PFOA, it was shown that neonatal exposure caused altered neuroprotein levels in the hippocampus and cerebral cortex in neonatal male mice. The present study show that neonatal exposure to PFHxS, during the peak of the brain growth spurt, can alter neuroprotein levels e.g. CaMKII, GAP-43, synaptophysin and tau, which are essential for normal brain development in mice. This was measured for both males and females, in hippocampus and cerebral cortex. The results suggest that PFHxS may act as a developmental neurotoxicant and the effects are similar to that of PFOS and PFOA, but also to other substances such as PCBs, PBDEs and Bisphenol A.

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Tyrosine phosphorylation of synaptophysin in synaptic vesicle recycling

Cited by 70 publications

References 51 publications

Neurobehavioral and Immunological Consequences of Prenatal Immune Activation in Rats. Influence of Antipsychotics

Neurobehavioral and Immunological Consequences of Prenatal Immune Activation in Rats. Influence of Antipsychotics

Synaptophysin and postsynaptic density protein 95 in the human prefrontal cortex from mid-gestation into early adulthood

A single neonatal exposure to perfluorohexane sulfonate (PFHxS) affects the levels of important neuroproteins in the developing mouse brain

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