Simulated ischaemia induces Ca<sup>2+</sup>‐independent glutamatergic vesicle release through actin filament depolymerization in area CA1 of the hippocampus

Andrade, Adriana L.; Rossi, David J.

doi:10.1113/jphysiol.2010.187609

Cited by 25 publications

(24 citation statements)

References 49 publications

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“…An increase in mEPSCs has been described previously at early phases of ischemia, before AD (33,38,41). The increase in mEPSC frequency was Ca 2+ independent and caused by ischemia-induced actin filament depolymerization (41). However, the increased spontaneous vesicular transmitter release caused by energy depletion only leads to extracellular glutamate accumulation when glial glutamate uptake is blocked (33).…”

Section: Discussionmentioning

confidence: 91%

“…Another possible source of glutamate is vesicular release. An increase in mEPSCs has been described previously at early phases of ischemia, before AD (33,38,41). The increase in mEPSC frequency was Ca 2+ independent and caused by ischemia-induced actin filament depolymerization (41).…”

Section: Discussionmentioning

confidence: 99%

“…An increase in vesicular synaptic glutamate release and in miniature excitatory postsynaptic currents (mEPSCs) occurs at early phases of ischemia and before AD (33,41,42). We therefore tested whether vesicular release was contributing to the increase in AD currents in acute slices by using bafilomycin A1 (Baf A1; 1 μM), a vacuolar type H + -ATPase inhibitor, to block neurotransmitter loading into synaptic vesicles.…”

Section: Introductionmentioning

confidence: 99%

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Extrasynaptic glutamate release through cystine/glutamate antiporter contributes to ischemic damage

Soria¹,

Pérez-Samartı́n²,

Martín³

et al. 2014

J. Clin. Invest.

110

112

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Section: Discussionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Extrasynaptic glutamate release through cystine/glutamate antiporter contributes to ischemic damage

Soria¹,

Pérez-Samartı́n²,

Martín³

et al. 2014

J. Clin. Invest.

110

112

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“…Preconditioning is associated with changes in the glutamatergic system, mainly increase in glutamate release through the non-Ca 2? -dependent mechanisms [130] associated with increased expression and activity of glutamate transporters [131] (see Fig. 6).…”

Section: Glutamate and Preconditioningmentioning

confidence: 99%

The role of glutamate in neuronal ischemic injury: the role of spark in fire

2011

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Although being a physiologically important excitatory neurotransmitter, glutamate plays a pivotal role in various neurological disorders including ischemic neurological diseases. Its level is increased during cerebral ischemia with excessive neurological stimulation causing the glutamate-induced neuronal toxicity, excitotoxicity, and this is considered the triggering spark in the ischemic neuronal damage. The glutamatergic stimulation will lead to rise in the intracellular sodium and calcium, and the elevated intracellular calcium will lead to mitochondrial dysfunction, activation of proteases, accumulation of reactive oxygen species and release of nitric oxide. Interruption of the cascades of glutamate-induced cell death during ischemia may provide a way to prevent, or at least reduce, the ischemic damage. Various therapeutic options are suggested interrupting the glutamatergic pathways, e.g., inhibiting the glutamate synthesis or release, increasing its clearance, blocking of its receptors or preventing the rise in intracellular calcium. Development of these strategies may provide future treatment options in the management of ischemic stroke.

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“…Chorein is particularly important for function and viability of neurons and skeletal muscle cells [6,11]. Moreover, chorein polymerizes cortical actin filaments [3,17], which is expected to affect a variety of cellular functions including exocytosis [3,60,61,62,63,64,65,66,67,68,69]. Along those lines several cytoskeletal structures including actin microfilaments, microtubules and desmin-, as well as cytokeratin-intermediate filaments are disorganized in human fibroblasts from chorea-acanthocytosis-patients [17].…”

Section: Discussionmentioning

confidence: 99%

Chorein Sensitive Dopamine Release from Pheochromocytoma (PC12) Cells

Honisch¹,

Fehrenbacher

Lebedeva

et al. 2015

Neurosignals

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Background: Chorein, a protein supporting activation of phosphoinositide 3 kinase (PI3K), participates in the regulation of actin polymerization and cell survival. A loss of function mutation of the chorein encoding gene VPS13A (vacuolar protein sorting-associated protein 13A) leads to chorea-acanthocytosis (ChAc), a neurodegenerative disorder with simultaneous erythrocyte akanthocytosis. In blood platelets chorein deficiency has been shown to compromise expression of vesicle-associated membrane protein 8 (VAMP8) and thus degranulation. The present study explored whether chorein is similarly involved in VAMP8 expression and dopamine release of pheochromocytoma (PC12) cells. Methods: Chorein was down-regulated by silencing in PC12 cells. Transmission electron microscopy was employed to quantify the number of vesicles, RT-PCR to determine transcript levels, Western blotting to quantify protein expression and ELISA to determine dopamine release. Results: Chorein silencing significantly reduced the number of vesicles, VAMP8 transcript levels and VAMP8 protein abundance. Increase of extracellular K⁺ from 5 mM to 40 mM resulted in marked stimulation of dopamine release, an effect significantly blunted by chorein silencing. Conclusions: Chorein deficiency down-regulates VAMP8 expression, vesicle numbers and dopamine release in pheochromocytoma cells.

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Simulated ischaemia induces Ca²⁺‐independent glutamatergic vesicle release through actin filament depolymerization in area CA1 of the hippocampus

Cited by 25 publications

References 49 publications

Extrasynaptic glutamate release through cystine/glutamate antiporter contributes to ischemic damage

Extrasynaptic glutamate release through cystine/glutamate antiporter contributes to ischemic damage

The role of glutamate in neuronal ischemic injury: the role of spark in fire

Chorein Sensitive Dopamine Release from Pheochromocytoma (PC12) Cells

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Simulated ischaemia induces Ca2+‐independent glutamatergic vesicle release through actin filament depolymerization in area CA1 of the hippocampus

Cited by 25 publications

References 49 publications

Extrasynaptic glutamate release through cystine/glutamate antiporter contributes to ischemic damage

Extrasynaptic glutamate release through cystine/glutamate antiporter contributes to ischemic damage

The role of glutamate in neuronal ischemic injury: the role of spark in fire

Chorein Sensitive Dopamine Release from Pheochromocytoma (PC12) Cells

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Simulated ischaemia induces Ca²⁺‐independent glutamatergic vesicle release through actin filament depolymerization in area CA1 of the hippocampus