2013
DOI: 10.1016/j.neuro.2013.07.009
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Quercetin inhibits depolarization-evoked glutamate release in nerve terminals from rat cerebral cortex

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Cited by 23 publications
(11 citation statements)
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“…Another compound - quercetin - was also shown to prevent depolarization-evoked Glu release from rat synaptosomes and, comparable to luteolin, decreased presynaptic voltage-dependent Ca 2+ entry by blocking Cav2.1 and Cav2.2. Moreover, this mechanism involved the simultaneous inhibition of both PKC and PKA activities, which by phosphorylation, regulate the activity of Ca 2+ channels [ 64 ].…”
Section: Glutamatergic Signaling and Poly-phenolsmentioning
confidence: 99%
“…Another compound - quercetin - was also shown to prevent depolarization-evoked Glu release from rat synaptosomes and, comparable to luteolin, decreased presynaptic voltage-dependent Ca 2+ entry by blocking Cav2.1 and Cav2.2. Moreover, this mechanism involved the simultaneous inhibition of both PKC and PKA activities, which by phosphorylation, regulate the activity of Ca 2+ channels [ 64 ].…”
Section: Glutamatergic Signaling and Poly-phenolsmentioning
confidence: 99%
“…This bioflavonoid has multiple neurobeneficial activities, such as free radical scavenging, antianxiety, neuroprotection, and cognitive enhancing effects. [191][192][193] Quercetin is chemo labile and thermo labile, which leads to lower bioavailability at the target site. 194 In addition, quercetin has poor solubility and distribution, resulting in less bioavailability to the brain.…”
Section: Nanoquercetinmentioning
confidence: 99%
“…Therefore, we prepared an animal model of chronic glaucoma and used this model to study the mechanism of quercetin’s neuroprotective effect at the presynaptic afferent level. As an important excitatory neurotransmitter of the central nervous system (CNS), glutamate plays an important role in synaptic plasticity, learning and memory (Greenamyre and Porter, 1994; Lu et al, 2013). In addition to physiological functions, glutamate in synaptic clefts has potential excitotoxicity after excessive release.…”
Section: Introductionmentioning
confidence: 99%
“…In addition to physiological functions, glutamate in synaptic clefts has potential excitotoxicity after excessive release. Excessive glutamate release is one of the molecular mechanisms responsible for many neuropathic neuron injuries, including acute traumatic stroke, seizures, and traumatic brain and spinal cord injury, and chronic neurodegenerative diseases such as Parkinson’s disease and Alzheimer’s disease (Lu et al, 2013). Therefore, effective reduction of glutamate release would be considered a potential neuroprotective strategy.…”
Section: Introductionmentioning
confidence: 99%
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