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Titolo:
Neurotrophin receptor TrkB activation is not required for the postnatal survival of retinal ganglion cells in vivo
Autore:
Rohrer, B; LaVail, MM; Jones, KR; Reichardt, LF;
Indirizzi:
Univ Calif San Francisco, Sch Med, Howard Hughes Med Inst, San Francisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA Univ Calif San Francisco, Sch Med, Beckman Vis Ctr, San Francisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA Univ Colorado, MCD Biol, Boulder, CO USA Univ Colorado Boulder CO USAUniv Colorado, MCD Biol, Boulder, CO USA
Titolo Testata:
EXPERIMENTAL NEUROLOGY
fascicolo: 1, volume: 172, anno: 2001,
pagine: 81 - 91
SICI:
0014-4886(200111)172:1<81:NRTAIN>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
MOUSE RETINA; IN-VIVO; AXONAL REGENERATION; SUPERIOR COLLICULUS; OXIDATIVE STRESS; GENE-EXPRESSION; GROWTH-FACTOR; OPTIC-NERVE; BRAIN; DEATH;
Keywords:
TrkB; retinal ganglion cell; optic nerve; myelination; neuroprotection;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
53
Recensione:
Indirizzi per estratti:
Indirizzo: Rohrer, B Med Univ S Carolina, Storm Eye Inst, Room 707,167 Ashley Ave, Charleston, SC 29425 USA Med Univ S Carolina Room 707,167 Ashley Ave Charleston SC USA 29425
Citazione:
B. Rohrer et al., "Neurotrophin receptor TrkB activation is not required for the postnatal survival of retinal ganglion cells in vivo", EXP NEUROL, 172(1), 2001, pp. 81-91

Abstract

During early postnatal development, apoptosis of retinal ganglion cells (RGCs) is regulated by target contact with the optic tectum. The neurotrophins BDNF and NT-4, but not NGF, prevent the apoptosis of retinal ganglion cells that is otherwise observed after target ablation or axotomy. Thus receptors activated by BDNF and NT-4 are candidates to mediate the early postnatal survival of RGCs. BDNF and NT-4, but not NGF, bind to all isoforms of thereceptor TrkB, whether or not they contain a tyrosine kinase domain. To examine the roles of TrkB receptor isoforms in early postnatal survival, we compared RGC numbers in wild-type mice to those in a mutant lacking all isoforms of TrkB. Surprisingly, no reduction in RGCs was observed in the mutantat postnatal day 16, the latest age at which these animals are consistently viable, so TrkB signaling is not essential for target-dependent survival of these cells. In wild-type mice, RGCs also are lost gradually during adulthood, possibly due to oxidative stress. To determine whether TrkB signaling regulates this phase of RGC degeneration, RGC numbers were examined in a viable mutant of TrkB that expresses only about 25% the normal level of TrkB receptor kinase. Compared to controls, approximately 20% of the RGC were lost in mutant 3-month-old-animals. Thus, TrkB signaling is not required for survival of RGCs during the period of target-dependent survival, but doesappear to reduce degeneration of RGCs in adult animals. (C) 2001 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 12:06:39