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Titolo:
BDNF increases the number of axotomized rat retinal ganglion cells expressing GAP-43, L1, and TAG-1 mRNA - A supportive role for nitric oxide?
Autore:
Klocker, N; Jung, M; Stuermer, CAO; Bahr, M;
Indirizzi:
Univ Tubingen, Dept Neurol, D-72076 Tubingen, Germany Univ Tubingen Tubingen Germany D-72076 Neurol, D-72076 Tubingen, Germany Univ Konstanz, Dept Biol, D-78457 Constance, Germany Univ Konstanz Constance Germany D-78457 Biol, D-78457 Constance, Germany
Titolo Testata:
NEUROBIOLOGY OF DISEASE
fascicolo: 1, volume: 8, anno: 2001,
pagine: 103 - 113
SICI:
0969-9961(200102)8:1<103:BITNOA>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
AXONAL GLYCOPROTEIN TAG-1; CENTRAL-NERVOUS-SYSTEM; NEUROTROPHIC FACTOR; NEURITE OUTGROWTH; PROTEIN GAP-43; ADULT-RATS; ADHESION MOLECULES; CEREBRAL-ISCHEMIA; RECEPTOR TRKB; UP-REGULATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
70
Recensione:
Indirizzi per estratti:
Indirizzo: Klocker, N Univ Tubingen, Dept Neurol, Hoppe Seyler Str 3, D-72076 Tubingen, Germany Univ Tubingen Hoppe Seyler Str 3 Tubingen Germany D-72076 many
Citazione:
N. Klocker et al., "BDNF increases the number of axotomized rat retinal ganglion cells expressing GAP-43, L1, and TAG-1 mRNA - A supportive role for nitric oxide?", NEUROBIOL D, 8(1), 2001, pp. 103-113

Abstract

The death of neurons and the limited ability to activate growth-associatedgenes prevent the restoration of lesioned fiber tracts in the adult mammalian CNS. Here, we characterized the effects of the survival-promoting neurotrophin brain-derived neurotrophic factor (BDNF) on mRNA expression of GAP-43, L1, TAG-1, and SC-1 in axotomized and regenerating rat retinal ganglioncells (RGCs). BDNF led to de novo upregulation of TAG-1 mRNA in axotomizedRGCs and to a threefold increase in the number of GAP-43 and L1 mRNA-expressing RGCs. SC-1 expression remained unchanged. However, BDNF did not improve long-distance axon regeneration into a peripheral nerve graft. Surprisingly, potentiating BDNF-mediated neuroprotection by simultaneous administration of a spin trap or a NOS inhibitor counteracted the BDNF-induced growth-associated gene expression. This led us to hypothesize that the BDNF effects on GAP-43, L1, and TAG-1 mRNA expression are mediated by a NO-dependent mechanism. In summary, our data support the idea that survival and axon regeneration of lesioned CNS neurons can be regulated independently. (C) 2001 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 07:03:22