2014
DOI: 10.1016/j.neuropharm.2014.06.009
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A novel multi-target ligand (JM-20) protects mitochondrial integrity, inhibits brain excitatory amino acid release and reduces cerebral ischemia injury in vitro and in vivo

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Cited by 46 publications
(31 citation statements)
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“…In this work we have observed that JM-20 inhibited glutamate uptake by synaptic vesicles in association with an inhibition of V-ATPase activity and a dissipation of ΔpH. These related effects may contribute to the reduction of glutamate quantal size, thus reducing the glutamate released into the synapses, and could partly explain the anti-excitotoxic effect we recently observed in vivo (Nuñez-Figueredo et al, 2014b).…”
Section: Discussionsupporting
confidence: 57%
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“…In this work we have observed that JM-20 inhibited glutamate uptake by synaptic vesicles in association with an inhibition of V-ATPase activity and a dissipation of ΔpH. These related effects may contribute to the reduction of glutamate quantal size, thus reducing the glutamate released into the synapses, and could partly explain the anti-excitotoxic effect we recently observed in vivo (Nuñez-Figueredo et al, 2014b).…”
Section: Discussionsupporting
confidence: 57%
“…We observed here that JM-20 enhanced glutamate uptake in astrocyte culture alone at very low micromolar concentrations, but it did not, in cortical neurons. Because the astrocytic glutamate transport plays a major role in maintaining extracellular glutamate concentrations below neurotoxic levels (Anderson and Swanson, 2000;Danbolt, 2001), and the neurotransmitter uptake by astrocytes can be stimulated by several neuroprotective compounds (Beller et al, 2011;Karki et al, 2014;Wu et al, 2008), the above mentioned effects of JM-20 may contribute to explain its anti-excitotoxic actions in vitro (Nuñez-Figueredo et al, 2014a) and in vivo (Nuñez-Figueredo et al, 2014b).…”
Section: Discussionmentioning
confidence: 99%
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“…In vivo, JM-20 treatment (4 and 8 mg/kg) significantly decreased neurological deficit scores, edema formation, total infarct volumes and histological alterations in different brain regions 13 . Rapamycin could improve brain edema progression after reperfusion injury through maintaining blood-brain barrier integrity and inhibiting metalloproteinase 9 and aquaporin 4 (AQP4) expression 14 .…”
Section: Red Neuron Countingmentioning
confidence: 90%
“…Similar findings were seen in rats submitted to short term (1h) IR (Figure 4). In vitro, a novel multi-target ligand (JM-20 -1 and 10 μM) administered during reperfusion significantly reduced cell death in hippocampal slices subjected to oxygen and glucose deprivation 13 .…”
Section: Red Neuron Countingmentioning
confidence: 97%