POSTNATAL CHANGES IN THE EXPRESSION OF THE TRKA HIGH-AFFINITY NGF RECEPTOR IN PRIMARY SENSORY NEURONS

Citation
Dlh. Bennett et al., POSTNATAL CHANGES IN THE EXPRESSION OF THE TRKA HIGH-AFFINITY NGF RECEPTOR IN PRIMARY SENSORY NEURONS, European journal of neuroscience, 8(10), 1996, pp. 2204-2208
Citations number
25
Categorie Soggetti
Neurosciences
ISSN journal
0953816X
Volume
8
Issue
10
Year of publication
1996
Pages
2204 - 2208
Database
ISI
SICI code
0953-816X(1996)8:10<2204:PCITEO>2.0.ZU;2-B
Abstract
In development similar to 70-80% of dorsal root ganglion (DRG) cells a re dependent on nerve growth factor (NGF) for their survival, while in the adult only some 40% of DRG cells express the high-affinity NGF re ceptor, trkA. This discrepancy suggests that trkA expression, and ther efore neurotrophin sensitivity, may alter as the animal matures. We ha ve tested this possibility by counting the number of L4/5 DRG neurons showing immunoreactivity for trkA in rats from the day of birth to pos tnatal day 14. We also examined changes in p75 and IB4 labelling. On t he day of birth, 71% of DRG cells were found to express trkA. However, this percentage gradually fell with age and reached adult levels at p ostnatal day 14. The expression of p75 did not parallel that of trkA, remaining relatively constant at between 45 and 50% of cells from birt h to postnatal day 14. Over the same period there was a marked increas e in the proportion of cells which bind the lectin IB4 from 9 (day of birth) to 40% (day 14). Since in the adult the IB4 population consists of small cells which mostly do not express trkA, this finding suggest s that the postnatal down-regulation of trkA occurs in this population . Consistent with this suggestion are the results of double labelling for trkA and IB4, which confirmed that at times intermediate between b irth and postnatal day 14 there was a high degree of coexpression betw een these markers (which is absent in the adult), This result also sug gests that the down-regulation of trkA is unlikely to be directly resp onsible for the emerging IB4 binding.