Regulation of neurotrophin receptors during the maturation of the mammalian visual system

Abstract

with the onset of cell death and maturation of axonal connections. This study demonstrates that members of the trk family, previously identified in the CNS on the basis of mRNA transcripts, are present as receptors with specific binding affinities for BDNF and NT-3. Moreover, the correspondence between the developmental shift from full-length to truncated trkB and the critical periods for cell fate determination, cell death, and axonal remodeling suggests an important role for neurotrophic factors in the development of the visual system.

A Truncated Tropo-Myosine-Related Kinase B Receptor, T1, Regulates Glial Cell Morphology via Rho GDP Dissociation Inhibitor 1

“…Rho GDI1 is a T1-binding protein T1 exhibits a characteristic developmental expression pattern in the mammalian CNS (i.e., the expression of T1 is known to be remarkably increased after birth and is a major product among TrkB subtypes in adults) (Allendoerfer et al, 1994;Fryer et al, 1996;Ohira et al, 1999). Thus, we purified T1-binding proteins from the cytosolic fraction of adult rat brains, using an affinity column conjugated with the C-terminal-specific sequence of T1.…”

“…For example, the expression of T1 increases markedly at various important periods in the developing mammalian CNS, such as axonal remodeling and synaptogenesis (Allendoerfer et al, 1994;Fryer et al, 1996;Ohira et al, 1999Ohira et al, , 2001. The specific alignment of the intracellular domain of T1 is completely identical among mice, rats, and humans (Klein et al, 1990;Middlemas et al, 1991;Shelton et al, 1995), suggesting that the alignment plays a unique role.…”

Stimulation of the neurotrophin receptor TrkB on astrocytes drives nitric oxide production and neurodegeneration

“…TrkB-T1 was up-regulated on astrocytes in EAE lesions as well. During mouse development, the expression of TrkB isoforms is tightly regulated in the CNS (Allendoerfer et al, 1994), and, interestingly, the shift from the full-length to the truncated isoform correlates with the onset of neuronal death and maturation of axonal connections (Allendoerfer et al, 1994;Ohira et al, 1999). A few studies demonstrate that dysregulation of TrkB isoforms in neurons may lead to cell death (Dorsey et al, 2002(Dorsey et al, , 2006.…”

Interaction of Survival and Death Signaling in Basal Forebrain Neurons: Roles of Neurotrophins and Proneurotrophins

“…To determine whether the neurons that expressed TrkB together with p75 NTR were among those that died in response to pro-NGF, neurons were grown on slide wells in the presence of BDNF for 5 d. BDNF was then readded to ensure that the TrkB receptor was activated, and cells were treated for 4 h with vehicle, mature NGF, or pro-NGF. Cells were then fixed and labeled with Hoechst dye to identify apoptotic cells by nuclear morphology, and double immunostained with antibodies to p75 NTR (192 IgG) and to either the full-length TrkB (TrkB in ) (Allendoerfer et al, 1994;Friedman, 2000) or P-Trk. TrkB in -positive neurons were identified, examined for p75 coexpression, and determined to be either healthy or apoptotic by nuclear morphology.…”