Protective effects of the free radical scavenger edaravone against glutamate neurotoxicity in nearly pure neuronal culture

Hisano, K.; Watanabe, Masahiko; Morimoto, Yuji

doi:10.1007/s00540-009-0766-z

Cited by 18 publications

(14 citation statements)

References 31 publications

(37 reference statements)

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“…We used affinity-purified primary antibodies raised against the following molecules (species immunized): MGL (rabbit; see below), DGL␣ [rabbit ], mGluR5 [guinea pig and goat (Uchigashima et al, 2007a)], MAP2 [rabbit and goat ], synaptophysin [guinea pig ], CB 1 receptor [guinea pig (Fukudome et al, 2004)], calretinin [mouse (MAB1568; Millipore Bioscience Research Reagents), rabbit (Miyazaki et al, 2011)], VGluT1 [rabbit and goat (Miyazaki et al, 2003;Miura et al, 2006)], VGluT2 [guinea pig and goat (Miyazaki et al, 2003;Miura et al, 2006)], vesicular inhibitory amino acid transporter [VIAAT; goat (Miyazaki et al, 2003;Miura et al, 2006)], vesicular acetylcholine transporter [VAChT; rabbit ], glial fibrillary acidic protein [GFAP; guinea pig (Hisano et al, 2009)], GLAST [goat (Shibata et al, 1997)], 2Ј,3Ј-cyclic nucleotide 3Ј phosphodiesterase (CNPase; mouse; C5922; Sigma), and Iba1 (rabbit; Wako). For production of the MGL antibody, a cDNA fragment encoding the N-terminal 35 amino acids (NCBI reference sequence NM_011844) was subcloned into BamHI/EcoRI site of pGEX4T-2 plasmid (GE Healthcare) for expression of glutathione S-transferase fusion proteins.…”

Section: Methodsmentioning

confidence: 99%

Molecular and Morphological Configuration for 2-Arachidonoylglycerol-Mediated Retrograde Signaling at Mossy Cell–Granule Cell Synapses in the Dentate Gyrus

Uchigashima¹,

Yamazaki²,

Yamasaki³

et al. 2011

J. Neurosci.

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2-Arachidonoylglycerol (2-AG) is the endocannabinoid that mediates retrograde suppression of neurotransmission in the brain. In the present study, we investigated the 2-AG signaling system at mossy cell (MC)-granule cell (GC) synapses in the mouse dentate gyrus, an excitatory recurrent circuit where endocannabinoids are thought to suppress epileptogenesis. First, we showed by electrophysiology that 2-AG produced by diacylglycerol lipase ␣ (DGL␣) mediated both depolarization-induced suppression of excitation and its enhancement by group I metabotropic glutamate receptor activation at MC-GC synapses, as they were abolished in DGL␣-knock-out mice. Immunohistochemistry revealed that DGL␣ was enriched in the neck portion of GC spines forming synapses with MC terminals, whereas cannabinoid CB 1 receptors accumulated in the terminal portion of MC axons. On the other hand, the major 2-AG-degrading enzyme, monoacylglycerol lipase (MGL), was absent at MC-GC synapses but was expressed in astrocytes and some inhibitory terminals. Serial electron microscopy clarified that a given GC spine was innervated by a single MC terminal and also contacted nonsynaptically by other MC terminals making synapses with other GC spines in the neighborhood. MGL-expressing elements, however, poorly covered GC spines, amounting to 17% of the total surface of GC spines by astrocytes and 4% by inhibitory terminals. Our findings provide a basis for 2-AG-mediated retrograde suppression of MC-GC synaptic transmission and also suggest that 2-AG released from activated GC spines is readily accessible to nearby MC-GC synapses by escaping from enzymatic degradation. This molecular-anatomical configuration will contribute to adjust network activity in the dentate gyrus after enhanced excitation.

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Section: Methodsmentioning

confidence: 99%

Molecular and Morphological Configuration for 2-Arachidonoylglycerol-Mediated Retrograde Signaling at Mossy Cell–Granule Cell Synapses in the Dentate Gyrus

Uchigashima¹,

Yamazaki²,

Yamasaki³

et al. 2011

J. Neurosci.

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“…The medium was changed every third day and the cells were grown for 14 days. A pilot study showed that the proportion of neurons among the cells was over 90% in our culture system [15].…”

Section: Methodsmentioning

confidence: 99%

“…The relative frequencies of apoptotic cells were examined after 24 h of hypoxia at 37, 33, and 30°C by the methods of Shimizu et al as described before [15]. The cells were stained for 30 min at 37°C with Hoechest 33342 (SigmaAldrich) and propidium iodide (Sigma-Aldrich).…”

Section: Percentages Of Viable Apoptotic and Necrotic Cellsmentioning

confidence: 99%

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Effect of mild and moderate hypothermia on hypoxic injury in nearly pure neuronal culture

Hisano

Morimoto

2010

J Anesth

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“…Recent studies on the mechanism of spinal cord injury suggest that free radicals affect the development of the spinal cord injury by enhancing partial ischemia-reperfusion injury (Sun et al, 2010;He et al, 2010;Wang et al, 2011). Edaravone is a radical scavenger (Uji et al, 2008;Hisano et al, 2009;Ye et al, 2011;Ono et al, 2011). The current study aimed to observe the effect of edaravone on the repair of rat spinal cord injury and to explore the potential of the combination of edaravone with neural stem cell (NSC) transplantation to treat spinal cord injury.…”

Section: Introductionmentioning

confidence: 94%

Combination of edaravone and neural stem cell transplantation repairs injured spinal cord in rats

Song¹,

Peng²,

Ye³

2015

Genet. Mol. Res.

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ABSTRACT. This study sought to observe the effect of the combination of edaravone and neural stem cell (NSC) transplantation on the repair of complete spinal cord transection in rats. Eighty adult female SpragueDawley (SD) rats were used to establish the injury model of complete spinal cord transection at T9. Animals were divided randomly into four groups (N = 20 each): control, edaravone, transplantation, and edaravone + transplantation. The recovery of spinal function was evaluated with the Basso, Beattie, Bresnahan (BBB) rating scale on days 1, 3, and 7 each week after the surgery. After 8 weeks, the BBB scores of the control, edaravone, transplantation, and combination groups were 4.21 ± 0.11, 8.46 ± 0.1, 8.54 ± 0.13, and 11.21 ± 0.14, respectively. At 8 weeks after surgery, the spinal cord was collected; the survival and transportation of transplanted cells were observed with PKH-26 labeling, and the regeneration and distribution of spinal nerve fibers with fluorescent-gold (FG) retrograde tracing. Five rats died due to the injury. PKH-26-labeled NSCs had migrated into the spinal cord. A few intact nerve fibers and pyramidal neurons passed the injured area in the transplantation and combination groups. The numbers Edaravone and neural stem cell transplantation in SCI 19137©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (4): 19136-19143 (2015) of PKH-26-labeled cells and FG-labeled nerve fibers were in the order: combination group > edaravone group and transplantation group > control group (P < 0.05 for each). Thus, edaravone can enhance the survival and differentiation of NSCs in injured areas; edaravone with NSC transplantation can improve the effectiveness of spinal cord injury repair in rats.

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Protective effects of the free radical scavenger edaravone against glutamate neurotoxicity in nearly pure neuronal culture

Cited by 18 publications

References 31 publications

Molecular and Morphological Configuration for 2-Arachidonoylglycerol-Mediated Retrograde Signaling at Mossy Cell–Granule Cell Synapses in the Dentate Gyrus

Molecular and Morphological Configuration for 2-Arachidonoylglycerol-Mediated Retrograde Signaling at Mossy Cell–Granule Cell Synapses in the Dentate Gyrus

Effect of mild and moderate hypothermia on hypoxic injury in nearly pure neuronal culture

Combination of edaravone and neural stem cell transplantation repairs injured spinal cord in rats

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