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Effects of postnatal anti‐NGF on the development of CGRP‐IR neurons in the dorsal root ganglion
Author(s) -
Tonra James R.,
Mendell Lorne M.
Publication year - 1998
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/(sici)1096-9861(19980323)392:4<489::aid-cne6>3.0.co;2-x
Subject(s) - calcitonin gene related peptide , dorsal root ganglion , nerve growth factor , medicine , biology , endocrinology , nociceptor , calcitonin , sensory system , nociception , population , sensory neuron , neuroscience , neuropeptide , receptor , environmental health
Experiments were undertaken to examine anatomical correlates of physiological effects of rabbit sera raised against nerve growth factor (anti‐NGF) on nociceptive afferents. This antiserum has been shown to deplete the population of A‐δ high threshold mechanoreceptors and to reduce neurogenic vasodilatation. Because numerous studies implicate calcitonin gene related peptide (CGRP)‐ containing sensory neurons in these effects, immunocytochemical and anatomical techniques were used to examine the normal development of CGRP‐immunoreactive (‐IR) neurons in the dorsal root ganglion (DRG) of rats from 13 days to 19 weeks of age, and to compare this to the development in rats treated neonatally (postnatal days 2‐14) with anti‐NGF. In controls the rate of increase in the mean diameter of CGRP‐IR cells was substantially greater between 13 days and 5 weeks of age than it was between 5 weeks and 19 weeks, in contrast to CGRP‐negative neurons whose rate of growth remained relatively constant. Anti‐NGF had no significant effect on growth rate, but rats treated with anti‐NGF exhibited a reduced proportion of CGRP‐IR neurons at 5 weeks. This deficit was reversed by 19 weeks unlike the physiological changes. These results indicate independent regulation of CGRP expression and nociceptor physiology by NGF. J. Comp. Neurol. 392: 489–498, 1998. © 1998 Wiley‐Liss, Inc.