Timing and regulation of trkB and BDNF mRNA expression in placode-derived sensory neurons and their targets.
The sensory neurons of the vestibular and nodose ganglia of the chicken embryo have nearby and distant targets, respectively. In vitro studies have shown that these neurons survive independently of neurotrophins when their axons are growing to their targets and become dependent on brain-derived neurotrophic factor (BDNF) for survival when their axons reach the vicinity of their targets. Although the timing of BDNF dependence is principally controlled by an intrinsic timing mechanism in the neurons, the onset of dependence can be accelerated by BDNF exposure toward the end of the phase of neurotrophin independence. We have used quantitative reverse transcription/polymerase chain reaction to study the expression of transcripts coding for BDNF and the catalytic isoform of its receptor tyrosine kinase, TrkB, in these neurons and their targets at different stages of development. We show that the peripheral and central target tissues of these neurons express BDNF mRNA prior to the arrival of sensory axons. Vestibular neurons express trkB mRNA before nodose neurons, which accords with the earlier response of vestibular neurons to BDNF. In culture, early nodose neurons start expressing trkB mRNA after 36 h incubation, which is 36 h before these neurons become dependent on BDNF for survival. Although BDNF does not affect the timing and level of trkB mRNA expression during the first 48 h in vitro, it increases the level of trkB mRNA after this time. The timing of BDNF-induced elevation of trkB mRNA correlates with the period during which BDNF exposure accelerates the onset of BDNF dependence in nodose neurons. These results suggest that the timing of BDNF dependence in developing sensory neurons is due in part to expression of catalytic TrkB and demonstrate that a BDNF autocrine loop is not required for the survival of sensory neurons during the earliest stages of their development.
Robinson
M
M
School of Biological and Medical Sciences, University of St Andrews, Fife, UK.
Adu
J
J
Davies
A M
AM
D000818:Animals; D001369:Axons / Q000502:physiology; D001483:Base Sequence; D019208:Brain-Derived Neurotrophic Factor / Q000096:biosynthesis*; D002470:Cell Survival; D002478:Cells, Cultured; D002642:Chick Embryo; D017931:DNA Primers; D018507:Gene Expression Regulation, Developmental; D009475:Neurons, Afferent / Q000166:cytology / Q000502:physiology*; D009620:Nodose Ganglion / Q000196:embryology / Q000378:metabolism*; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000096:biosynthesis; D020794:Receptor Protein-Tyrosine Kinases / Q000096:biosynthesis*; D020801:Receptor, Ciliary Neurotrophic Factor; D017475:Receptors, Nerve Growth Factor / Q000096:biosynthesis*; D012249:Rhombencephalon / Q000196:embryology / Q000378:metabolism*; D013997:Time Factors; D014158:Transcription, Genetic; D014722:Vestibule, Labyrinth / Q000196:embryology / Q000294:innervation
D019208:Brain-Derived Neurotrophic Factor; D017931:DNA Primers; D012333:RNA, Messenger; D020801:Receptor, Ciliary Neurotrophic Factor; D017475:Receptors, Nerve Growth Factor; D020794:Receptor Protein-Tyrosine Kinases