About: Synaptophysin is a research topic. Over the lifetime, 2922 publications have been published within this topic receiving 122382 citations. The topic is also known as: MRX96 & MRXSYP.
TL;DR: A polypeptide of Mr 38,000 has been identified as a specific component of the membrane of presynaptic vesicles, using the monoclonal antibody SY38, and this protein, for which the name synaptophysin*, is proposed, provides a molecular marker for the presyspheric membrane and may be involved in synaptic vesicle formation and exocytosis.
TL;DR: NACP sequence showed 95% identity with that of rat synuclein 1, a synaptic/nuclear protein previously identified in rat brain, and good homology with Torpedo syn DNA from the electric organ synapse and bovine phosphoneuroprotein 14 (PNP-14), a brain-specific protein present in synapses, suggesting that synaptic aberration observed in senile plaques might be involved in amyloidogenesis in Alzheimer's disease.
TL;DR: It is shown that the onset of α- and β-synuclein expression was delayed after synaptic development, suggesting that these synucleins may not be essential for synapse formation, and that one function ofα- synuclein may be to regulate the size of distinct pools of synaptic vesicles in mature neurons.
Abstract: alpha-, beta-, and gamma-Synuclein, a novel family of neuronal proteins, has become the focus of research interest because alpha-synuclein has been increasingly implicated in the pathogenesis of Parkinson's and Alzheimer's disease. However, the normal functions of the synucleins are still unknown. For this reason, we characterized alpha-, beta-, and gamma-synuclein expression in primary hippocampal neuronal cultures and showed that the onset of alpha- and beta-synuclein expression was delayed after synaptic development, suggesting that these synucleins may not be essential for synapse formation. In mature cultured primary neurons, alpha- and beta-synuclein colocalized almost exclusively with synaptophysin in the presynaptic terminal, whereas little gamma-synuclein was expressed at all. To assess the function of alpha-synuclein, we suppressed expression of this protein with antisense oligonucleotide technology. Morphometric ultrastructural analysis of the alpha-synuclein antisense oligonucleotide-treated cultures revealed a significant reduction in the distal pool of synaptic vesicles. These data suggest that one function of alpha-synuclein may be to regulate the size of distinct pools of synaptic vesicles in mature neurons.
TL;DR: Immunohistochemistry in human and rat brain revealed widespread cytoplasmic labeling of huntingtin within neurons, rather than the more selective pattern of axon terminal labeling characteristic of many vesicle-associated proteins.
TL;DR: Levels of synaptotagmin and GAP43 were unchanged in mild AD, but cases with CDR of >1 had a progressive decrement in these synaptic proteins, indicating that synaptic injury in frontal cortex is an early event in AD.
Abstract: The expression levels of three synaptic proteins (synaptophysin, synaptotagmin, and growth-associated protein 43 [GAP43]) in AD cases clinically classified by Clinical Dementia Rating (CDR) score were analyzed. Compared with control subjects (CDR = 0), mild (early) AD (CDR = 0.5 to 1) cases had a 25% loss of synaptophysin immunoreactivity. Levels of synaptotagmin and GAP43 were unchanged in mild AD, but cases with CDR of >1 had a progressive decrement in these synaptic proteins. Thus, synaptic injury in frontal cortex is an early event in AD.