001     136271
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024 7 _ |a 10.1007/s00441-011-1200-z
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024 7 _ |a pmc:PMC3132349
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024 7 _ |a 0044-3794
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024 7 _ |a 0302-766X
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024 7 _ |a 0340-0336
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024 7 _ |a 0373-031X
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037 _ _ |a DZNE-2020-02593
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Ehninger, Dan
|0 P:(DE-2719)2289209
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|e First author
245 _ _ |a Enriched environment and physical activity reduce microglia and influence the fate of NG2 cells in the amygdala of adult mice.
260 _ _ |a Heidelberg
|c 2011
|b Springer
264 _ 1 |3 online
|2 Crossref
|b Springer Science and Business Media LLC
|c 2011-06-21
264 _ 1 |3 print
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|b Springer Science and Business Media LLC
|c 2011-07-01
336 7 _ |a article
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336 7 _ |a ARTICLE
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520 _ _ |a Proliferative cells expressing proteoglycan neuron-glia 2 (NG2) are considered to represent parenchymal precursor cells in the adult brain and are thought to differentiate primarily into oligodendrocytes. We have studied cell genesis in the adult amygdala and found that, up to 1 year after the labeling of proliferating cells with bromodeoxyuridine, most proliferating NG2 cells remain NG2 cells, and only a few slowly differentiate into mature oligodendrocytes, as assessed by the expression of 2',3'-cyclic nucleotide 3'-phosphodiesterase. We have detected no signs of neurogenesis but have confirmed the expression of 'neuronal' markers such as Doublecortin in NG2 cells. Nestin-expressing NG2 cells in the amygdala show electrophysiological properties known for oligodendrocyte precursor cells in the corpus callosum. Application of the glutamate agonist kainate elicits a 'complex' response consisting of a rapid and long-lasting blockade of the resting K(+) conductance, a transient cationic current, and a transient increase of an outwardly directed K(+) conductance, suggesting the responsiveness of NG2 cells to excitation. Proliferation of NG2 cells increases in response to behavioral stimuli of activity, voluntary wheel running, and environmental enrichment. In addition to reducing the number of newborn microglia, behavioral activity results in a decrease in S100β-expressing newborn NG2 cells in the amygdala. Because S100β expression in NG2 cells ceases with oligodendrocyte maturation, this finding suggests that NG2 cells in the amygdala undergo activity-dependent functional alterations, without resulting in a measurable increase in new mature oligodendrocytes over the time period covered by the present study. The adult amygdala thus shows signs of mixed activity-dependent plasticity: reduced numbers of microglia and, presumably, an altered fate of NG2 cells.
536 _ _ |a 342 - Disease Mechanisms and Model Systems (POF3-342)
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650 _ 7 |a Nerve Growth Factors
|2 NLM Chemicals
650 _ 7 |a S100 Calcium Binding Protein beta Subunit
|2 NLM Chemicals
650 _ 7 |a S100 Proteins
|2 NLM Chemicals
650 _ 7 |a Bromodeoxyuridine
|0 G34N38R2N1
|2 NLM Chemicals
650 _ 2 |a Aging: physiology
|2 MeSH
650 _ 2 |a Amygdala: cytology
|2 MeSH
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Bromodeoxyuridine: metabolism
|2 MeSH
650 _ 2 |a Cell Count
|2 MeSH
650 _ 2 |a Cell Line
|2 MeSH
650 _ 2 |a Cell Lineage
|2 MeSH
650 _ 2 |a Cell Proliferation
|2 MeSH
650 _ 2 |a Electrophysiological Phenomena
|2 MeSH
650 _ 2 |a Environment
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Microglia: cytology
|2 MeSH
650 _ 2 |a Microglia: metabolism
|2 MeSH
650 _ 2 |a Motor Activity
|2 MeSH
650 _ 2 |a Nerve Growth Factors: metabolism
|2 MeSH
650 _ 2 |a Neurogenesis
|2 MeSH
650 _ 2 |a Neurons: cytology
|2 MeSH
650 _ 2 |a Neurons: metabolism
|2 MeSH
650 _ 2 |a Oligodendroglia: cytology
|2 MeSH
650 _ 2 |a Oligodendroglia: metabolism
|2 MeSH
650 _ 2 |a Phenotype
|2 MeSH
650 _ 2 |a S100 Calcium Binding Protein beta Subunit
|2 MeSH
650 _ 2 |a S100 Proteins: metabolism
|2 MeSH
650 _ 2 |a Visual Cortex: cytology
|2 MeSH
650 _ 2 |a Visual Cortex: metabolism
|2 MeSH
700 1 _ |a Wang, Li-Ping
|b 1
700 1 _ |a Klempin, Friederike
|b 2
700 1 _ |a Römer, Benedikt
|b 3
700 1 _ |a Kettenmann, Helmut
|b 4
700 1 _ |a Kempermann, Gerd
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773 1 8 |a 10.1007/s00441-011-1200-z
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|t Cell and Tissue Research
|v 345
|y 2011
|x 0302-766X
773 _ _ |a 10.1007/s00441-011-1200-z
|g Vol. 345, no. 1, p. 69 - 86
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856 4 _ |y OpenAccess
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856 7 _ |2 Pubmed Central
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21