Glucose/oxygen deprivation induces the alteration of synapsin I and phosphosynapsin

Jung, Yong-Taek; Park, Su Jin; Lee, Jun Young

doi:10.1016/j.brainres.2003.09.069

Cited by 26 publications

(34 citation statements)

References 37 publications

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“…A decrease in the number of SVs per terminal could also point to an impairment of SV recycling process. It has been shown in many studies that SV proteins change their phosphorylation level under physiological and pathological conditions (Genoud et al, 1999;Bolay et al, 2002;Jung et al, 2004). SNAP-25, synapsin, synaptotagmins, and mint1, which are all implicated in the regulation of synaptic transmission and SV cycling, have been reported to be modified either in their expression level or their phosphorylation following transient ischemia (Nishimura et al, 2000;Ishimaru et al, 2001;Nakajima et al, 2001;Yokota et al, 2001;Bolay et al, 2002;Jung et al, 2004).…”

Section: Discussionmentioning

confidence: 98%

Ischemia-induced modifications in hippocampal CA1 stratum radiatum excitatory synapses

et al. 2006

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Relatively mild ischemic episode can initiate a chain of events resulting in delayed cell death and significant lesions in the affected brain regions. We studied early synaptic modifications after brief ischemia modeled in rats by transient vessels' occlusion in vivo or oxygen-glucose deprivation in vitro and resulting in delayed death of hippocampal CA1 pyramidal cells. Electron microscopic analysis of excitatory spine synapses in CA1 stratum radiatum revealed a rapid increase of the postsynaptic density (PSD) thickness and length, as well as formation of concave synapses with perforated PSD during the first 24 h after ischemic episode, followed at the long term by degeneration of 80% of synaptic contacts. In presynaptic terminals, ischemia induced a depletion of synaptic vesicles and changes in their spatial arrangement: they became more distant from active zones and had larger intervesicle spacing compared to controls. These rapid structural synaptic changes could be implicated in the mechanisms of cell death or adaptive plasticity. Comparison of the in vivo and in vitro model systems used in the study demonstrated a general similarity of these early morphological changes, confirming the validity of the in vitro model for studying synaptic structural plasticity.

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Section: Discussionmentioning

confidence: 98%

Ischemia-induced modifications in hippocampal CA1 stratum radiatum excitatory synapses

et al. 2006

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“…In cultured hippocampal slices at least 30-min OGD has been previously applied to induce ischemic neuronal death [8,14,15], and up to an hour and more [16,17,18,19,20]. Such long-term OGD is known to cause significant neuronal damage.…”

Section: Discussionmentioning

confidence: 99%

Morphological and functional changes in rat hippocampal slice cultures after short‐term oxygen‐glucose deprivation

Lushnikova

Воронин

Malyarevskyy

et al. 2004

J Cellular Molecular Medi

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To study effects of short‐term cerebral ischemia, hippocampal slice cultures were subjected to oxygen and glucose deprivation (OGD) followed by a period of normoxic reoxygenation. Propidium iodide staining, and MTT/formazanassay were used to evaluate cell viability and metabolic activity. CA1 pyramidal cells were analyzed at the light‐and electron microscopic levels. Cell damage was found to be insignificant during the first hour after 10 min OGD but profound following 4 h, showing delayed neuronal cell damage caused by short‐term OGD. Our model can be used to characterize the mechanisms of cell damage caused by mild cerebral ischemia. These data might apply to further development of neuroprotective tools for the treatment of brain diseases.

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“…In their study, conducted on a model of Parkinson's disease, they demonstrated that REST down-regulated synapsin 1. Other authors have demonstrated that synapsin 1 is activated in hippocampus exposed to ischemic injury as part of a plastic adaptation mechanism (Jung et al, 2004). All of this evidence suggests that synapsin 1 could represent a marker of neurodegeneration because it is involved in the modulation of neurotransmitter release and synaptic vesicle reclustering (Nemani et al, 2010).…”

Section: Downloaded Frommentioning

confidence: 98%

“…For instance, evidence has shown that synapsin 1, one of the REST target genes regulated by histone deacetylase (HDAC), is involved in the pathogenesis of some neurocognitive disorders (Wu et al, 2007) and neurodegenerative diseases (Jung et al, 2004). Accordingly, we hypothesized that this gene could serve as a possible mediator of PCB-induced neurocognitve alterations.…”

Section: A-1254 Increased the Expression Of Both Corest And Msin3a Trmentioning

confidence: 98%

The Repressor Element 1-Silencing Transcription Factor Is a Novel Molecular Target for the Neurotoxic Effect of the Polychlorinated Biphenyl Mixture Aroclor 1254 in Neuroblastoma SH-SY5Y Cells

Formisano

Guida

Cocco

et al. 2011

J Pharmacol Exp Ther

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Chronic exposure to polychlorinated biphenyls (PCBs), a class of ubiquitous environmental toxicants, causes neurocognitive anomalies. The transcription factor repressor element 1-silencing transcription factor (REST) plays a critical role in neuronal phenotype elaboration in both neural progenitor cells and non-neuronal cells. Here, we investigated the possible relationship between PCBs and REST in neuroblastoma SH-SY5Y cells. In these cells, chronic exposure to the PCB mixture Aroclor 1254 (A-1254; 5-30 μg/ml) caused dose-dependent cell death via the induction of calpain but not caspase-3. Intriguingly, this effect was prevented by the calpain inhibitor calpeptin. Furthermore, A-1254 enhanced REST mRNA and protein expression levels after both 24 and 48 h. REST down-regulation by small interfering RNA prevented A-1254-induced cell death. In addition, A-1254 enhanced the binding of REST to the synapsin 1 gene promoter, and synapsin 1 knockdown potentiated A-1254-induced cell death. A-1254 (10 μg/ml) also increased the expression of the two REST cofactors, the REST corepressor and the mammalian SIN3 homolog A transcription regulator. Moreover, the PCB mixture decreased acetylation of the histone proteins H3 and H4. It is noteworthy that the histone deacetylase inhibitor trichostatin A prevented such decreases and reduced the A-1254-induced neurotoxic effect. Collectively, these results suggest that A-1254 exerts its toxic effect via REST by down-regulating synapsin 1 and decreasing H3 and H4 acetylation.

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Glucose/oxygen deprivation induces the alteration of synapsin I and phosphosynapsin

Cited by 26 publications

References 37 publications

Ischemia-induced modifications in hippocampal CA1 stratum radiatum excitatory synapses

Ischemia-induced modifications in hippocampal CA1 stratum radiatum excitatory synapses

Morphological and functional changes in rat hippocampal slice cultures after short‐term oxygen‐glucose deprivation

The Repressor Element 1-Silencing Transcription Factor Is a Novel Molecular Target for the Neurotoxic Effect of the Polychlorinated Biphenyl Mixture Aroclor 1254 in Neuroblastoma SH-SY5Y Cells

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