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Upregulation of GFRα‐1 and c‐ret in primary sensory neurons and spinal motoneurons of aged rats
Author(s) -
Bergman Esbjörn,
Kullberg Susanna,
Ming Yu,
Ulfhake Brun
Publication year - 1999
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19990715)57:2<153::aid-jnr1>3.0.co;2-a
Subject(s) - glial cell line derived neurotrophic factor , neuroscience , sensory system , biology , dorsal root ganglion , gdnf family of ligands , downregulation and upregulation , neurotrophin , axon , proto oncogene proteins c ret , neurotrophic factors , sensory neuron , trk receptor , receptor tyrosine kinase , receptor , signal transduction , microbiology and biotechnology , biochemistry , gene
Aging is associated with a decline in neuromuscular and somatosensory functions. Senile muscle atrophy, considered to be of neurogenic origin, is prevalent, and sensory thresholds increase with age. However, the loss of motoneurons and primary sensory neurons is small, while sensory and motor innervation appears disturbed due to aging‐related axon lesions. One mechanism which may play a role in this process is altered trophin signaling. We here report that the glial cell line‐derived neurotrophic factor (GDNF) receptor GFRα‐1 mRNA and GFRα‐1 protein‐like immunoreactivity are upregulated in spinal motoneurons, and in dorsal root ganglion neurons of 30‐month‐old rats. The established signaling mechanism for the GDNF/GFRα‐1 complex is through binding to the tyrosine kinase receptor encoded by the c‐ret proto‐oncogene, and we also show here that c‐ret mRNA is upregulated in both motoneurons and primary sensory neurons of aged rats. The findings reported here, combined with evidence presented in other studies of changes in p75 NTR and trk receptor expressions in aging primary sensory neurons and motoneurons, point at marked alterations in trophin signaling in senescence. J. Neurosci. Res. 57:153–165, 1999. © 1999 Wiley‐Liss, Inc.