Cellular neuroscienceCo-expression of the P75 neurotrophin receptor and neurotrophin receptor-interacting melanoma antigen homolog in the mature rat brain
Section snippets
Animals and treatment
Rats of the Sprague-Dawley and Dark Agouti strains, of both sexes, were used. Sprague-Dawley rats were obtained from the Walter and Eliza Hall Animal Facility (Melbourne, Australia), and Dark Agouti rats from the Australian Research Council Animal Facility (Adelaide, Australia). Rats were housed in groups of two or three on a 12-h light/dark cycle with food and water available ad libitum. Animals aged 1, 3, 6, 12, 17, and 26 months were killed and perfused, and their brains were removed.
Basal forebrain
Specificity of the NRAGE antiserum was confirmed by Western blotting brain lysate from a mature rat (Fig. 1). Initial studies showed strong NRAGE immunoreactivity in the basal forebrain of 1-month and older rats, and this appeared to be neuronal (Fig. 2A). There were no NRAGE-positive stellate cell profiles, suggesting an absence of astrocytic expression. To test our impression that NRAGE was exclusively neuronal, sections through the basal forebrain of adult mouse brain were double-stained for
Discussion
Motivated by recent findings that implicate NRAGE as an important factor in p75NTR signaling, the present study was undertaken to look for evidence of co-expression of NRAGE and p75NTR in neurons of the mature rat brain. NRAGE was found to be expressed in virtually all neurons that expressed p75NTR. In the stratum oriens of the hippocampal formation, the frequency of NRAGE and p75NTR-positive neurons was roughly equivalent. In other areas, such as the dentate gyrus, medial septum, and the VDB
Acknowledgments
This work was supported by the National Health and Medical Research Council of Australia.
References (39)
- et al.
Medial septal cholinergic neurons express c-Jun but do not undergo DNA fragmentation after fornix-fimbria transections
Brain Res Mol Brain Res
(1996) - et al.
NGF receptor reexpression and NGF-mediated cholinergic neuronal hypertrophy in the damaged adult neostriatum
Neuron
(1989) - et al.
Impaired spatial learning in aged rats is associated with loss of p75-positive neurons in the basal forebrain
Neuroscience
(2000) - et al.
Expression of the p75 neurotrophin receptor by striatal cholinergic neurons following global ischemia in rats is associated with neuronal degeneration
Neurosci Lett
(2002) - et al.
The low affinity NGF receptor, p75, can collaborate with each of the Trks to potentiate functional responses to the neurotrophins
Neuron
(1994) - et al.
Expression of p75(NTR), trkB and trkC in nonmanipulated and axotomized motoneurons of aged rats
Brain Res Mol Brain Res
(1999) - et al.
Neurotrophin receptor-interacting mage homologue is an inducible inhibitor of apoptosis protein-interacting protein that augments cell death
J Biol Chem
(2001) - et al.
Expression analysis of a novel p75(NTR) signaling protein, which regulates cell cycle progression and apoptosis
Mech Dev
(2002) - et al.
Immunohistochemical localization of cells containing nerve growth factor receptors in the different regions of the adult rat forebrain
Neuroscience
(1988) - et al.
Focal cerebral ischemia in rats induces expression of P75 neurotrophin receptor in resistant striatal cholinergic neurons
Neuroscience
(1998)
Localization of nerve growth factor, trkA and P75 immunoreactivity in the hippocampal formation and basal forebrain of adult rats
Neuroscience
The nerve growth factor family of receptors
Trends Neuroscie
Neurotrophin receptors in the somatosensory cortex of the mature ratco-localization of p75, trk, isoforms and c-neu
Brain Res
Distribution of nerve growth factor receptor-like immunoreactivity in the adult rat central nervous system. Effect of colchicine and correlation with the cholinergic system: I. Forebrain
Neuroscience
P75 neurotrophin receptor in the nucleus basalis of Meynert in relation to age, sex, and Alzheimer’s disease
Exp Neurol
NRAGE, a novel MAGE protein, interacts with the p75 neurotrophin receptor and facilitates nerve growth factor-dependent apoptosis
Neuron
NRAGE, a p75 neurotrophin receptor-interacting protein, induces caspase activation and cell death through a JNK-dependent mitochondrial pathway
J Biol Chem
Nerve growth factor receptor is associated with cholinergic neurons of the basal forebrain but not the pontomesencephalon
Neuroscience
The p75 nerve growth factor receptor mediates survival or death depending on the stage of sensory neuron development
Proc Natl Acad Sci USA
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2009, Molecular and Cellular ProteomicsCitation Excerpt :However, there is little information about p75NTR-mediated signaling by MAGED1. Because the localization of MAGED1 is not consistent with that of p75NTR (53), MAGED1 is likely to have the potential for signaling that is independent of p75NTR. Human MAGED1 reportedly regulates homotypic cell-cell adhesion by disrupting the E-cadherin·β-catenin complex (54).