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1 xposing these mutants and normal siblings to cuprizone.
2 could be carefully controlled using a toxin, cuprizone.
3 and IGF-1 tg mice 3 weeks after exposure to cuprizone.
5 ain during cuprizone toxicity, mice were fed cuprizone and evaluated at 3-, 4-, and 6-week cuprizone
6 demyelination by feeding the copper chelator cuprizone, and correlated our results with detailed hist
7 phodiesterase-EGFP(+) mice were treated with cuprizone, and OPCs were sorted from the corpus callosum
8 chronically demyelinated lesions induced by cuprizone appears to be the result of oligodendrocyte de
22 nd Th17 CD4(+) T cells infiltrate the CNS of cuprizone-fed mice, with infiltration of Th17 cells bein
25 d with that in wild-type mice in response to cuprizone feeding, demonstrating the essential role of I
26 lly demyelinated lesion of mice treated with cuprizone for 12 weeks, mature oligodendrocyte regenerat
27 cuprizone for 27 days and mice that were fed cuprizone for 25 days, followed by normal diet for 2 day
28 brains from control mice, mice that were fed cuprizone for 27 days and mice that were fed cuprizone f
29 dant in the brains of mice that had consumed cuprizone for 27 days, and the numbers of O4-positive ce
31 ollowing exposure to the demyelinating agent cuprizone, however, GALC +/- animals had significantly r
32 ecific chelators (bathocuproine disulfonate, cuprizone) induced nondesensitizing NMDAR currents even
33 ntiation in fibronectin aggregate containing cuprizone-induced demyelinated lesions in male mice.
35 trated that n-3 PUFA supplementation reduced cuprizone-induced demyelination and improved motor and c
36 the Nlrp3 gene was increased >100-fold in a cuprizone-induced demyelination and neuroinflammation mo
37 eceptor (CXCR2) were relatively resistant to cuprizone-induced demyelination and that circulating CXC
40 ly study its effects on remyelination in the cuprizone-induced demyelination model and in experimenta
42 the present study, we used a murine model of cuprizone-induced demyelination to broaden the applicati
43 l delay, myelination at the onset and during cuprizone-induced demyelination was unaffected in male N
44 ans with multiple sclerosis and of mice with cuprizone-induced demyelination, in ex vivo models of de
46 Our findings support a two-hit process of cuprizone-induced demyelination, supporting the idea tha
55 tion followed by longitudinal studies in the cuprizone-induced demyelination/remyelination mouse mode
56 tive demyelinating MS lesions, as well as in cuprizone-induced lesions, and that this phosphorylation
58 SOCS3-deficient mice were protected against cuprizone-induced oligodendrocyte loss relative to wild-
62 the brain to 40 Gy of X-irradiation prior to cuprizone intoxication and this resulted in a significan
63 lammatory protein-1alpha (MIP-1alpha) during cuprizone intoxication, a model where demyelination of t
69 ment of an innovative animal model combining cuprizone-mediated demyelination with transfer of myelin
76 (-/-) and Nlrp3(-/-) mice are studied in the cuprizone model of neuroinflammation and demyelination.
79 in the repair of a demyelinating lesion, the cuprizone model was used and the corpus callosum was exa
82 lin pathology in primary cultures and in the cuprizone mouse model of multiple sclerosis (MS), a deva
85 ormal diet following 12 weeks of exposure to cuprizone, remyelination and oligodendrocyte regeneratio
90 n vivo on an 11.7T animal MRI scanner from 7 cuprizone-treated and 7 control capital ES, Cyrillic57BL
92 ong-term locomotor performance of previously cuprizone-treated animals was monitored using the motor
95 e found that OPC-targeted Notch1 ablation in cuprizone-treated Plp-creER Notch1(lox/lox) transgenic m
96 uprizone and evaluated at 3-, 4-, and 6-week cuprizone treatment and 3- and 5-week post-cuprizone wit
97 on of pharmacological HDAC inhibitors during cuprizone treatment and is consistent with in vitro resu
98 on of pharmacological HDAC inhibitors during cuprizone treatment and is consistent with in vitro resu
99 reased as a function of dose and duration of cuprizone treatment and it was detectable prior to obser
111 emyelination mediated by the copper chelator cuprizone, we evaluated the expression of CXCL12 and its
112 on microscopy determined that at 3-week post-cuprizone withdrawal the number of dystrophic axons and
113 nificantly more SMI-32+ axons at 3-week post-cuprizone withdrawal, indicative of axonal damage in the
115 lial activation and astrogliosis, and, after cuprizone withdrawal, this activation reproducibly dimin
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