Identification and localization of synaptophysin, an integral membrane glycoprotein of Mr 38,000 characteristic of presynaptic vesicles

Wiedenmann, Bertram; Franke, Werner W.

doi:10.1016/s0092-8674(85)80082-9

Cited by 1,367 publications

(795 citation statements)

References 37 publications

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“…Similar to our results, Eastwood et al (2006) did not find any evidence for an adolescence--related decline in basal hippocampal synaptophysin expression, as it is seen, for example, in cortical brain areas (Glantz et al, 2007; but see also Webster et al, 2011). In as much as synaptophysin can be considered a presynaptic marker (Elferink and Scheller, 1995;Wiedenmann and Franke, 1985), our findings presented here, together with those reported by Eastwood et al (2006), suggest that the overall presynaptic density in the hippocampus is not reduced but rather increased between pubescence and adulthood.…”

supporting

confidence: 91%

“…The assessment of synaptic proteins included synaptophysin, bassoon, synaptic Ras GTPase--activating protein 1 (SynGAP), and postsynaptic density protein 95 (PSD95). Synaptophysin and bassoon are two major presynaptic proteins that are localized in or associated with presynaptic vesicles (Elferink and Scheller, 1995;Schoch and Gundelfinger, 2006;Shin, 2014;Wiedenmann and Franke, 1985). On the other hand, SynGAP and PSD95 are two major postsynaptic proteins that are enriched at postsynaptic sites of excitatory synapses, where they critically help organizing and strengthening excitatory receptor complexes and their associated signaling proteins (Kim et al, 1998;Kim and Sheng, 2004;Sheng and Hoogenraad, 2007).…”

Section: Introductionmentioning

confidence: 99%

“…Synaptophysin is one of the most widely used synaptic markers, which is typically taken to index synaptic integrity and presynaptic density (Elferink and Scheller, 1995;Wiedenmann and Franke, 1985). Synaptophysin is already expressed during early neuronal differentiation, where it appears to have important roles in synapse formation (Eastwood et al, 2006;Friedman et al, 2000;Zai et al, 2000).…”

mentioning

confidence: 99%

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Prenatal immune activation causes hippocampal synaptic deficits in the absence of overt microglia anomalies

Giovanoli

Weber‐Stadlbauer

Schedlowski

et al. 2016

Brain, Behavior, and Immunity

126

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Prenatal exposure to infectious or inflammatory insults can increase the risk of developing neuropsychiatric disorder in later life, including schizophrenia, bipolar disorder, and autism. These brain disorders are also characterized by pre-and postsynaptic deficits. Using a well-established mouse model of maternal exposure to the viral mimetic polyriboinosinic-polyribocytidilic acid [poly(I:C)], we examined whether prenatal immune activation might cause synaptic deficits in the hippocampal formation of pubescent and adult offspring. Based on the widely appreciated role of microglia in synaptic pruning, we further explored possible associations between synaptic deficits and microglia anomalies in offspring of poly(I:C)-exposed and control mothers. We found that prenatal immune activation induced an adult onset of presynaptic hippocampal deficits (as evaluated by synaptophysin and bassoon density). The early-life insult further caused postsynaptic hippocampal deficits in pubescence (as evaluated by PSD95 and SynGAP density), some of which persisted into adulthood. In contrast, prenatal immune activation did not change microglia (or astrocyte) density, nor did it alter their activation phenotypes. The prenatal manipulation did also not cause signs of persistent systemic inflammation. Despite the absence of overt glial anomalies or systemic inflammation, adult offspring exposed to prenatal immune activation displayed increased hippocampal IL-1 levels. Taken together, our findings demonstrate that age-dependent synaptic deficits and abnormal pro-inflammatory cytokine expression can occur during postnatal brain maturation in the absence of microglial anomalies or systemic inflammation. AbstractPrenatal exposure to infectious or inflammatory insults can increase the risk of developing neuropsychiatric disorder in later life, including schizophrenia, bipolar disorder, and autism. These brain disorders are also characterized by pre--and postsynaptic deficits.Using a well--established mouse model of maternal exposure to the viral mimetic polyriboinosinic--polyribocytidilic acid [poly(I:C)], we examined whether prenatal immune activation might cause synaptic deficits in the hippocampal formation of pubescent and adult offspring. Based on the widely appreciated role of microglia in synaptic pruning, we further explored possible associations between synaptic deficits and microglia anomalies in offspring of poly(I:C)--exposed and control mothers. We found that prenatal immune activation induced adult onset of presynaptic hippocampal deficits (as evaluated by synaptophysin and bassoon density). The early--life insult further caused postsynaptic hippocampal deficits in pubescence (as evaluated by PSD95 and SynGAP density), some of which persisted into adulthood. In contrast, prenatal immune activation did not change microglia (or astrocyte) density, nor did it alter their activation phenotypes. The prenatal manipulation did also not cause signs of persistent systemic inflammation. Despite the absence of overt glial a...

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supporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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Prenatal immune activation causes hippocampal synaptic deficits in the absence of overt microglia anomalies

Giovanoli

Weber‐Stadlbauer

Schedlowski

et al. 2016

Brain, Behavior, and Immunity

126

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“…p38/synaptophysin is a membrane protein present in clear (synaptic) vesicles of neurons and endocrine cells [1][2][3][4]. From the amino acid sequence deduced from cDNAs encoding p38/synaptophysin, a model with several membrane spanning polypeptide segments and a carboxy-terminal protein domain exposed to the cytoplasmic surface has been constructed [5][6][7].…”

Section: Introductionmentioning

confidence: 99%

Quantification of p38/synaptophysin in highly purified adrenal medullary chromaffin vesicles

Schilling

Gratzl

1988

FEBS Letters

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Chromaffin vesicles were first purified by differential and density gradient centrifugation in isotonic (Percoll) gradients. In subsequent sucrose gradients p38/synaptophysin exhibited the same distribution as established marker substances of chromaffin vesicles. Quantification of immunoblots revealed that 750 ng p38/synaptophysin per mg of protein were present in the chromaffin vesicles recovered from the sucrose gradient. Thus the amount of p38/synaptophysin per mg protein of chromaffin vesicles is about 100 times lower than that observed in clear (synaptic) vesicles. However, because of the large difference in surface area and protein content, the amount of p38/synaptophysin per single vesicle is the same in both types of organelles.p38/synaptophysin; Secretory vesicle; Immunoblotting; Quantification; (Adrenal medulla)

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“…Synaptophysin is a glycoprotein present in the membrane of pre-synaptic vesicles (Wiedenmann et al 1985).…”

Section: Characterisation Of Enteric Neuronal K V 14 Localisationmentioning

confidence: 99%

The role of humoral autoimmunity in gastrointestinal neuromuscular diseases

Hubball

Martin

Lang

et al. 2009

Progress in Neurobiology

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Dysfunction of the gastrointestinal neuromuscular apparatus (including interstitial cells ofCajal) is presumed to underlie a heterogeneous group of disorders collectively termed gastrointestinal neuromuscular diseases (GINMDs). Humoral (antibody)-mediated autoimmunity directed against ligand-or voltage-gated ion channels or associated proteins involved in neuromuscular transmission is associated with several acquired neuromuscular diseases of the periphery and is now implicated in an increasing number of less well-characterised diseases. Anti-channel antibodies have been reported in small numbers of patients with GINMD, particularly in those with GI dysfunction secondary to an underlying disease such as neoplasia or infection. However, little is known of humoral autoimmunity in primary GINMDs.This thesis investigated the association between anti-channel antibodies and GINMD, and the human GI tract as a potential target of anti-channel antibodies. The presence of antivoltage-and ligand-gated antibodies was investigated in the serum of patients with primary achalasia, enteric dysmotility and intestinal pseudo-obstruction, and in those with GINMD secondary to Chagas' disease. The functional effect of sera from some of these patients on colonic smooth muscle contractility was also characterised. Finally, the distribution of six voltage-gated potassium channels (VGKCs), which serve essential roles in the peripheral and central nervous systems and are known targets of pathological autoantibodies, were investigated in all layers of the human GI tract.Our findings suggest that currently recognised anti-channel antibodies are not a common pathogenic factor in primary GINMDs. Anti-channel antibodies, in particular anti-VGKC antibodies, were however found in a significant number of individuals with Chagas' disease. Furthermore, circulating factors in patients with chagasic GI disease altered GI smooth muscle contractility in vitro which may have pathological relevance to GI

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Identification and localization of synaptophysin, an integral membrane glycoprotein of Mr 38,000 characteristic of presynaptic vesicles

Cited by 1,367 publications

References 37 publications

Prenatal immune activation causes hippocampal synaptic deficits in the absence of overt microglia anomalies

Prenatal immune activation causes hippocampal synaptic deficits in the absence of overt microglia anomalies

Quantification of p38/synaptophysin in highly purified adrenal medullary chromaffin vesicles

The role of humoral autoimmunity in gastrointestinal neuromuscular diseases

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