ライフサイエンスコーパス: excitotoxin

1 e neuronal cell death even in the absence of excitotoxin.

2 ly related to the convulsant effects of this excitotoxin.

3 oxic, or enhances neuronal susceptibility to excitotoxins.

4 cells unilaterally using microinjections of excitotoxins.

5 levels did not change in the presence of the excitotoxins.

6 r agonists are powerful chemoconvulsants and excitotoxins.

7 trauma such as axonal damage and exposure to excitotoxins.

8 erebral infarct is thought to be mediated by excitotoxins.

9 striatal damage induced by the mitochondrial excitotoxin, 3-nitropropionic acid (3-NP).

10 susceptibility to the neurotoxic effects of excitotoxin administration is strain dependent.

11 To expose retinal ganglion cells (RGCs) to excitotoxins, adult CB6F1 mice were injected intravitrea

12 s were produced by multiple infusions of the excitotoxin AMPA.

13 , memory, and neuronal cell death induced by excitotoxin and ischemia.

14 of ischaemic and degenerative damage due to excitotoxins and consequent generation of free radicals,

15 t rather via a complex network of cytokines, excitotoxins, and free radical mechanisms triggered by h

16 ns, exacerbate the metabolic effects of this excitotoxin as well; in this case, the steroid manipulat

17 could be simulated in nontransgenic mice by excitotoxin challenge and prevented in hAPP mice by bloc

18 During excitotoxin challenge in the mouse hippocampus, neuron i

19 ar pathway, stimulating microglia to release excitotoxins, cytokines and reactive oxygen species, whi

20 d even if administered only 10 min following excitotoxin exposure.

21 nolinic acid, a macrophage/microglia-derived excitotoxin fulfills a plethora of functions such as neu

22 temic infusion (10 mg/kg body weight) of the excitotoxin; furthermore, the peptide protected even if

23 The Ca(2+) ionophore ionomycin and the excitotoxin glutamate induced production of p29 in cultu

24 levels of several amino acids, including the excitotoxins glutamate and aspartate, and further implic

25 In cultured primary cortical neurons, excitotoxins, hypoxic stress and calcium influx induce t

26 rate both before and after injections of the excitotoxin ibotenic acid into the most caudal part of t

27 f the amygdala and hippocampus made with the excitotoxin ibotenic acid, and then assessed their recog

28 own substrate for tPA, are also resistant to excitotoxins, implicating an extracellular proteolytic c

29 contrast (DIC) microscopy after exposure to excitotoxins in the presence or absence of (+)-PTZ.

30 observed following ischemia and produced by excitotoxins in vivo and in vitro.

31 onditions, the type of cell death induced by excitotoxins in vivo and the basis for the differential

32 cutaneous injection of kainic acid, a potent excitotoxin, induced comparable seizures in both wild-ty

33 aB (NF-kappaB) appears to participate in the excitotoxin-induced apoptosis of striatal medium spiny n

34 for nerve growth factor, contributes to the excitotoxin-induced apoptotic death of cholinergic neuro

35 increased ATP concentrations, and prevented excitotoxin-induced ATP depletion.

36 pin is due to inhibition of plasmin-mediated excitotoxin-induced cell death and is independent of neu

37 protein, protects neurons from ischemia and excitotoxin-induced damage.

38 F1R in forebrain neurons in mice exacerbated excitotoxin-induced death and neurodegeneration.

39 hat overexpression of p75 contributes to the excitotoxin-induced death of rat basal forebrain choline

40 hat NF kappa B activation contributes to the excitotoxin-induced death of striatal neurons.

41 ults in resistance of hippocampal neurons to excitotoxin-induced degeneration, and of striatal neuron

42 ient (plg(-/-)) mice, which are resistant to excitotoxin-induced degeneration.

43 Excitotoxin-induced destruction of striatal neurons, pro

44 the matrix, versus the striosomes, to early excitotoxin-induced DNA damage in rat striatum.

45 entazocine, had no neuroprotective effect on excitotoxin-induced ganglion cell death.

46 mice, previously identified as resistant to excitotoxin-induced hippocampal cell death, are resistan

47 g the neuronal cell death response following excitotoxin-induced injury.

48 the contribution of apoptotic mechanisms to excitotoxin-induced neurodegeneration as well as to char

49 ough tPA(-/-) mice are normally resistant to excitotoxin-induced neurodegeneration, disruption of the

50 en-deficient mice also display resistance to excitotoxin-induced neurodegeneration, in contrast with

51 not apoE4, protects against age-related and excitotoxin-induced neurodegeneration, we analyzed apoE

52 ir response may not be sufficient to prevent excitotoxin-induced neurodegeneration.

53 CSF1 and IL-34 strongly reduced excitotoxin-induced neuronal cell loss and gliosis in wi

54 E3, but not of apoE4, protected against this excitotoxin-induced neuronal damage.

55 These results indicate that excitotoxin-induced neuronal death and BBB breakdown are

56 lasmin cascade promotes neurodegeneration in excitotoxin-induced neuronal death, in inflammatory cond

57 hippocampus is not toxic and does not affect excitotoxin-induced neuronal death.

58 y identified as mediating a critical step in excitotoxin-induced neuronal death.

59 Thus, tau reduction can block Abeta- and excitotoxin-induced neuronal dysfunction and may represe

60 ed MMP activity may offer protection against excitotoxin-induced retinal damage.

61 in circulating cells strongly protected from excitotoxin-induced seizures, BBB leakage, CNS injury, a

62 during transient focal cerebral ischemia and excitotoxin-induced seizures.

63 st that apoptotic mechanisms are involved in excitotoxin-induced striatal cell death.

64 he neurons in plg(-/-) mice do not die after excitotoxin injection, BBB breakdown occurs to a similar

65 ssed in the hippocampus and disappears after excitotoxin injection.

66 ptic protection in vivo when coinjected with excitotoxin into the dorsal hippocampus.

67 mitotic neurons exposed to the glutamatergic excitotoxin kainate and promotes their apoptosis.

68 yramidal neurons after administration of the excitotoxin kainate.

69 In this study we administered the excitotoxin kainic acid (KA) to generate reactive oxygen

70 in hippocampal cultures challenged with the excitotoxin kainic acid (KA).

71 only in CA1 explants, and the glutamatergic excitotoxin kainic acid disrupting metabolism only in CA

72 e vector significantly protected against the excitotoxin kainic acid.

73 nt of hippocampal slices in culture with the excitotoxin, kainic acid, also produced calpain-mediated

74 The excitotoxin, kainic acid, was injected into the rostral

75 ites were measured: quinolinic acid (QA), an excitotoxin; kynurenic acid (KA), a neuroprotective rece

76 Using an excitotoxin lesion strategy, we explored the subcellular

77 ortex and olfactory bulb, with or without an excitotoxin lesion.

78 g acute (30 min) restraint was diminished by excitotoxin lesions of the ventral subiculum, a componen

79 Neuropathological consequences of excitotoxin lesions of the vHPC were investigated in thi

80 Small excitotoxin lesions were made using quinolinic acid at b

81 mechanical trauma of the nervous system, and excitotoxins, mainly by reducing apoptosis.

82 intracortical microinjection of the indirect excitotoxin malonate (500 nmol/0.5 microl) on days 1, 3

83 We have investigated this question using an excitotoxin-mediated brain injury model system, in conju

84 plasminogen activator (tPA) are resistant to excitotoxin-mediated hippocampal neuronal degeneration.

85 reactive oxygen species scavenger, prevented excitotoxin-mediated impairment of RVD.

86 dy, the role of matrix metalloproteinases in excitotoxin-mediated retinal damage was investigated.

87 Treatment of co-cultures with the excitotoxin N-methyl-D-aspartate (NMDA) induced neuronal

88 rotein kinase inhibitor staurosporine or the excitotoxin N-methyl-D-aspartate (NMDA).

89 he establishment of baseline responding, the excitotoxin N-methyl-D-aspartic acid (NMDA) was bilatera

90 ure of neurons to DNA damaging agents or the excitotoxin NMDA elicited similar results suggesting tha

91 olateral amygdaloid complex (with either the excitotoxin NMDA or the GABAA agonist muscimol) reduced

92 ax gene were damaged severely by exposure to excitotoxins or by the induction of DNA damage.

93 n that neuronal death induced by exposure to excitotoxins or to staurosporine was not attenuated.

94 nal damage produced by anoxia, ischemia, and excitotoxins present in food.

95 After chemical lesions, by using either the excitotoxin quinolinic acid (QA) or the complex II mitoc

96 of mitochondrial complex II activity or the excitotoxin quinolinic acid (QA).

97 Three metabolites were measured: the excitotoxin quinolinic acid (QA); the protective recepto

98 ion did not increase the release of the NMDA excitotoxin quinolinic acid (QUIN) from mononuclear cell

99 DIC examination of cells exposed to excitotoxins revealed substantial disruption of neuronal

100 that c-Myc and p53 induction occurred in the excitotoxin-sensitive medium-sized striatal neurons.

101 We show that ZIP4 is upregulated after excitotoxin stimulation of the mouse, male and female, h

102 ion elicited through exogenous insults (e.g. excitotoxins, stroke) is promoted by an extracellular ca

103 egeneration after intracerebral injection of excitotoxins such as glutamate, and neuronal damage afte

104 SOD-1) transgenic mice and mice treated with excitotoxins supports a role for excitotoxicity in the m

105 h d-Phe44 is significantly more active as an excitotoxin than the l-Phe analogue both in vitro and in

106 This pathway results in quinolinate, an excitotoxin that is an NMDA receptor agonist.

107 Adaptation to the continued presence of excitotoxins that potentiate NMDARs such as HIV Tat may

108 Since quinolinic acid acts as a potent excitotoxin, the early depolarizing response in GABAergi

109 xic challenges such as hypoxia-hypoglycemia, excitotoxin treatment or metabolic inhibition of culture

110 exhibited little or no damage in response to excitotoxin treatment.

111 ppocampal neuronal susceptibility to HIV/MDM excitotoxins varies according to the developmental expre

112 tabolism that can act as an endogenous brain excitotoxin when released by activated macrophages.