TY  - JOUR
A1  - ,  
T1  - Insulin-like growth factor 1-receptor (IGF-1R) in developing and adult human dorsal root ganglia
JO  - Eur. J. Anat.
SN  - 1136-4890
Y1  - 2000
VL  - 4
SP  - 185
EP  - 190
UR  - http://www.eurjanat.com/web/paper.php?id=00030185
KW  - somatomedin C receptor
KW  - adult
KW  - article
KW  - cell differentiation
KW  - cell maturation
KW  - cell size
KW  - embryo
KW  - fetus
KW  - glia cell
KW  - human
KW  - human tissue
KW  - immunohistochemistry
KW  - immunoreactivity
KW  - protein localization
KW  - Schwann cell
KW  - sensory nerve cell
KW  - spinal cord nerve cell
KW  - spinal ganglion
N2  - Insulin-like growth factors (IGFs) promote neurite outgrowth in cultured sensory neurons that binding to IGF type 1 receptor (IGF-1R) and seem to be involved in the pathogenesis of some metabolic and toxic peripheral neuropathies coursing with altered sensitivity. However, the distribution of IGF-1R in the human sensory peripheral nervous system is unknown. In this study, we used light immunohistochemistry to analyse the occurrence and localization of IGF-1R in developing (6 to 22 weeks of estimated gestational age, e.g.a.) and adult (age range 25-41 years) human dorsal root ganglia (DRG). In human embryos (6-8 weeks e.g.a.) and young foetuses (9 weeks e.g.a.), most neurons (84%, 92%, and 83%, respectively) displayed IGF-1R immunoreactivity (IR). In older foetuses (12 and 22 weeks e.g.a.), the number of immunoreactive neurons decreased progressively (78 and 68%, respectively) reaching values similar to those observed in adults (64%). The subpopulation of adult primary sensory neurons showing IGF-1R IR covered the entire size range, but the neurons were mainly small. Furthermore, in adults all satellite glial cells and Schwann cells were immunoreactive. The present results suggest a role for IGF-1R in the differentiation and maturation of primary sensory neurons, and in the maintenance of a subset of them in adulthood, as well as in the control of peripheral glial cells (Schwann and satellite glial cells). These findings might serve as a basis for future studies in pathologic DRG, in which IGF-1R or its ligands may be involved.
ER  -