| First Author | Silos-Santiago I | Year | 1995 |
| Journal | J Neurosci | Volume | 15 |
| Issue | 9 | Pages | 5929-42 |
| PubMed ID | 7666178 | Mgi Jnum | J:28575 |
| Mgi Id | MGI:76098 | Doi | 10.1523/JNEUROSCI.15-09-05929.1995 |
| Citation | Silos-Santiago I, et al. (1995) Non-TrkA-expressing small DRG neurons are lost in TrkA deficient mice. J Neurosci 15(9):5929-42 |
| abstractText | Experiments over the past decade in which NGF/TrkA signaling has been abolished by antibodies or targeted gene mutations have shown that 70-85% of dorsal root ganglion (DRG) neurons require NGF for survival during development. There is consensus that many of the NGF-dependent neurons are small-diameter, peptidergic neurons subserving nociception. These neurons express the signaling receptor for NGF, TrkA. There is a major discrepancy, however, between the percentage of DRG neurons which require NGF for survival (70-85%) and percentage of DRG neurons expressing TrkA receptors (40-50%). The identity of these non-TrkA expressing, NGF-dependent neurons has not been established. A candidate group is a population of small DRG neurons with unmyelinated axons which bind BSI isolectins from the plant, Bandeiraea simplicifolia. We show here that most of these BSI-binding DRG neurons do not express TrkA in adult mice. However, in mutant mice in which NGF/TrkA signaling has been abolished by inactivation of the trkA gene, BSI-staining in the DRG and dorsal horn is completely eliminated. BSI-binding DRG cells are thus the first identified neuronal population in which cells do not express TrkA in maturity, but require NGF/TrkA signaling for survival during embryonic development. These neurons must either depend on NGF via a novel, indirect mechanism or alternatively, downregulate TrkA expression during development. |
