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1 lpha inhibitors as potent protectors against glutamate toxicity.
2 abilities to protect retinal neurons against glutamate toxicity.
3  in turn heightens neuronal vulnerability to glutamate toxicity.
4 osure to oxygen-glucose deprivation (OGD) or glutamate toxicity.
5 y improves the resistance of MILS neurons to glutamate toxicity.
6 preconditioning of neurons against Abeta and glutamate toxicity.
7 I; blocking IL-1beta may usefully counteract glutamate toxicity.
8 val and protection of glial progenitors from glutamate toxicity.
9 r neuron degeneration, both based in part on glutamate toxicity.
10 tase inhibitors, 17beta-estradiol attenuated glutamate toxicity.
11 ceptors protected motor neurons from chronic glutamate toxicity.
12 ns from hydrogen peroxide and nonexcitotoxic glutamate toxicity.
13 tor and markedly increases susceptibility to glutamate toxicity.
14 n in rat primary cortical neurons exposed to glutamate toxicity.
15 of the hippocampal slice preparation against glutamate toxicity.
16 neuropathological conditions associated with glutamate toxicity.
17 tive oxygen species from mitochondria during glutamate toxicity.
18 y a variety of reagents that block oxidative glutamate toxicity.
19 ed excitotoxicity can be caused by oxidative glutamate toxicity.
20 e and a form of cell injury called oxidative glutamate toxicity.
21 mature primary cortical neuron cultures from glutamate toxicity.
22 tion and impaired [Ca2+]c homeostasis during glutamate toxicity.
23 ured primary neurons were also salvaged from glutamate toxicity.
24  the deregulation of [Ca2+]i associated with glutamate toxicity.
25 -derived neurotrophic factor (BDNF) prevents glutamate toxicity.
26 e toxicity, and exogenous PC-PLC potentiates glutamate toxicity.
27 , memantine was partially protective against glutamate toxicity.
28 tecting ganglion cells from chronic low-dose glutamate toxicity.
29  agents that block monoamine uptake inhibits glutamate toxicity.
30                                In a model of glutamate toxicity, activation of SK2 channels attenuate
31                                              Glutamate toxicity after activation of N-methyl-D-aspart
32                      Inhibitors of sGC block glutamate toxicity and a cGMP analogue potentiates cell
33 fficient strategy to prevent the detrimental glutamate toxicity and further studies are warranted to
34 aying a role in the subsequent inducement of glutamate toxicity and loss of proline neuroprotective e
35 olism and demonstrate a relationship between glutamate toxicity and monoamine metabolism.
36 rgent molecular and cellular defects such as glutamate toxicity and neuronal loss.
37 impulse transmission include nodal widening, glutamate toxicity, and disturbances of both the blood-b
38          A PC-PLC inhibitor blocks oxidative glutamate toxicity, and exogenous PC-PLC potentiates glu
39 us mechanisms including oxidative stress and glutamate toxicity, and occurs in both MS patients and i
40 heir ability to protect cells from oxidative glutamate toxicity, and protection appears to take place
41 d mitochondrial potential (DeltaPsim) during glutamate toxicity, and to define the mechanisms underly
42 eath following BDNF withdrawal may be due to glutamate toxicity, as the N-methyl-d-aspartate (NMDA) r
43  and mature cells (5+ days in vitro) against glutamate toxicity, but its precise mechanism is still u
44 eurons and spinal cord motor neurons against glutamate toxicity, but the protection was lost in neuro
45       Thus, this cytokine appears to prevent glutamate toxicity by a mechanism unrelated to a blockad
46 hesis and release of BDNF, which may prevent glutamate toxicity by an autocrine loop.
47 chniques, we examined whether IL-10 prevents glutamate toxicity by blocking the function of NMDA chan
48                                        Since glutamate toxicity caused by EAAT2 dysfunction is though
49 uring neurons a protective mechanism against glutamate toxicity during development.
50 nterleukin-1 receptor antagonist (IL-1ra) in glutamate toxicity following SCI.
51 onses, and strongly increased sensitivity to glutamate toxicity in cell culture.
52 ite on the NMDA receptor and protect against glutamate toxicity in cultured hippocampal neurons.
53 e neurotrophin-mediated neuroprotection from glutamate toxicity in cultured neurons at 2 weeks in vit
54 articles containing TRH was assessed against glutamate toxicity in cultured rat fetal hippocampal neu
55 lar signal-regulated kinases-1/2 (ERK1/2) in glutamate toxicity in HT22 cells and immature embryonic
56 2/15-LOX and is protective against oxidative glutamate toxicity in mouse neuronal HT22 cells.
57   Understanding of the mechanisms underlying glutamate toxicity in multiple sclerosis could help in t
58 uggested to be responsible for counteracting glutamate toxicity in neuronal human-derived SH-SY5Y cel
59  provide new insights into the mechanisms of glutamate toxicity in neurons.
60 europrotective effect of TRH/analogs against glutamate toxicity in primary hippocampal neuronal cultu
61         Here, we suggest the need to explore glutamate toxicity in the context of specific disease mo
62 brinal, induces resistance against oxidative glutamate toxicity in the hippocampal cell line HT22 and
63     However, haloperidol effectively blocked glutamate toxicity in the same cultures, suggesting that
64  also protected mitochondrial function under glutamate toxicity, including maintaining mitochondrial
65                     We also demonstrate that glutamate toxicity involves a combination of ferroptosis
66          One of the key questions concerning glutamate toxicity is how a transient NMDA exposure can
67                                              Glutamate toxicity is inhibited by monoamine oxidase (MA
68 ment of neurodegenerative disorders in which glutamate toxicity is thought to be involved.
69             Previous studies have shown that glutamate toxicity may be prevented by antioxidants.
70                 Recent studies indicate that glutamate toxicity may involve the c-Jun amino-terminal
71 rs expressed on axons, or indirectly through glutamate toxicity of myelin or neighboring glial cells.
72 ns that were subjected to potassium removal, glutamate toxicity, or 6-hydroxydopamine treatment and f
73 es caspase-independent cell death induced by glutamate toxicity, oxidative stress, hypoxia, or ischem
74 neuron cultures subjected to AMPA-R-mediated glutamate toxicity suffered up to 40% less damage than u
75 ic nerve, elevated intraocular pressure, and glutamate toxicity, the immune modulator glatiramer acet
76         These results suggest that oxidative glutamate toxicity toward neurons lacking functional NMD
77 ovide evidence that in a neuronal cell line, glutamate toxicity via the oxidative pathway requires mo
78            Moreover, FGF1 protection against glutamate toxicity was dependent on GSK3beta inactivatio
79 erability of cultured hippocampal neurons to glutamate toxicity was greater in cells lacking gelsolin
80       In experiments in which the potency of glutamate toxicity was increased by the transport inhibi
81                                              Glutamate toxicity was induced for 1, 3, 6, and 24 h to
82 ibitors, 17beta-estradiol protection against glutamate toxicity was lost.
83                                              Glutamate toxicity was reduced by both cannabidiol, a no
84 ole of ROS in cell death caused by oxidative glutamate toxicity was studied in an immortalized mouse
85 Using a spinal cord culture model of chronic glutamate toxicity, we show herein that a synthetic 44 m
86 s of PEDF against both induced apoptosis and glutamate toxicity were blocked by the addition of eithe
87 f ROS production and protect HT22 cells from glutamate toxicity when added early in the death program
88            Mutant neurons are susceptible to glutamate toxicity, which can be rescued pharmacological
89                                 In oxidative glutamate toxicity, which is distinct from excitotoxicit