Abstract：
:Neurosphere-forming cells (NSFCs) derived from primary cultures of adult human olfactory epithelium were established in minimum essential medium (MEM) with Hanks balanced salts and 10% heat-inactivated fetal bovine serum (FBS). A totally defined medium (DM) was employed to examine their proliferation, lineage restriction and differentiation. DMEM/F12 (DF) was found to support NSFCs and served as the base medium for this study. NSFCs were adapted to the DM through serial serum reductions at successive feedings. NSFCs in DF supplemented with N2, B27 or insulin attained saturation density and formed extensive processes. Immunolocalization of lineage specific markers [i.e., nestin, beta-tubulin III, peripherin, neural cell adhesion molecule, A2B5, O4, microtubule-associated-protein-2 (MAP2) and glial fibrillary acidic protein], as well as 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide and ornithine decarboxylase assays were employed to characterize the NSFCs. The effects of trophic factors including epidermal growth factor (EGF), nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), ciliary neurotrophic factor (CNTF), neurotrophic factors (NT-3), and basic fibroblast growth factor (bFGF) were evaluated. With the reduction of serum and the addition N2, B27, and other nutrients, there was a change in lineage restriction including an increase the expression of A2B5 and other glial markers as well as the expression of mature neuronal markers with a simultaneous reduction of nestin reactivity. NSFCs proliferated and maintained their pluripotency for over a year in the DM. Further studies will determine the utility of NSFCs for cell replacement therapy.
journal_name
Exp Neuroljournal_title
Experimental neurologyauthors
Zhang X,Klueber KM,Guo Z,Lu C,Roisen FJdoi
10.1016/j.expneurol.2003.10.022keywords:
subject
Has Abstractpub_date
2004-04-01 00:00:00pages
112-23issue
2eissn
0014-4886issn
1090-2430pii
S0014488603005545journal_volume
186pub_type
杂志文章abstract：:To ascertain whether signaling due to peripheral inflammation affects motoneuron vulnerability, we examined in adult rats the reaction to axonal injury of facial motoneurons primed by muscle inflammation. In this double-hit paradigm, preconditioning was achieved by injections into the facial muscles of the T cell mito...
journal_title：Experimental neurology
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pub_type： 杂志文章,评审
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journal_title：Experimental neurology
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journal_title：Experimental neurology
pub_type： 杂志文章
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journal_title：Experimental neurology
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journal_title：Experimental neurology
pub_type： 杂志文章
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更新日期：1988-07-01 00:00:00
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journal_title：Experimental neurology
pub_type： 杂志文章
doi：10.1006/exnr.2000.7551
更新日期：2001-02-01 00:00:00
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journal_title：Experimental neurology
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doi：10.1016/j.expneurol.2006.01.023
更新日期：2006-07-01 00:00:00
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pub_type： 杂志文章
doi：10.1016/j.expneurol.2020.113373
更新日期：2020-09-01 00:00:00
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journal_title：Experimental neurology
pub_type： 杂志文章
doi：10.1016/j.expneurol.2008.07.002
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doi：10.1016/j.expneurol.2014.03.006
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journal_title：Experimental neurology
pub_type： 杂志文章
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journal_title：Experimental neurology
pub_type： 杂志文章
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journal_title：Experimental neurology
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更新日期：1998-10-01 00:00:00
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journal_title：Experimental neurology
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abstract：:Nitric oxide may be a key mediator of excitotoxic neuronal injury in the central nervous system. In the present experiments we found that S-methylthiocitrulline, a relatively selective neuronal nitric oxide synthase (NOS) inhibitor, produced significant neuroprotection against striatal lesions produced by malonate, an...
journal_title：Experimental neurology
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journal_title：Experimental neurology
pub_type： 杂志文章
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更新日期：1985-08-01 00:00:00
abstract：:Granule cell (GC) neurogenesis increases following seizures, and some newborn GCs develop in abnormal locations within the hilus. These ectopic GCs (EGCs) display robust spontaneous and evoked excitatory activity. However, the pattern of afferent input they receive has not been fully defined. This study used electron ...
journal_title：Experimental neurology
pub_type： 杂志文章
doi：10.1016/j.expneurol.2005.08.007
更新日期：2005-12-01 00:00:00
