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Analysis of trkB-/-; trkC-/- double mutant mice revealed that peripheral and central inner ear sensory neurons are affected in these mice. However, a substantial amount of cochlear and vestibular neurons survive, possibly due to maintenance or upregulation of TrkA expression. To clarify the function of the TrkA receptor during development of the cochlear and vestibular ganglion we analysed trkA-/- mice and the expression of this receptor in inner ear sensory neurons of trkB-/-; trkC-/- animals. TrkA homozygous mutant mice showed normal numbers of neurons and no TrkA expression was detected in neurons of trkB-/-; trkC-/- double mutant mice. We conclude that TrkA is not essential for inner ear development and that in the absence of any of the known catalytic Trk receptors peripheral inner ear sensory neurons are prone to undergo cell death or must use a different signaling mechanism to survive.

Type

Journal

Mech Dev

Publication Date

06/1997

Volume

64

Pages

77 - 85

Keywords

Animals, Base Sequence, Cell Survival, Cochlea, DNA Primers, Ear, Inner, In Situ Hybridization, Mice, Mice, Knockout, Neurons, Afferent, Phenotype, Proto-Oncogene Proteins, Receptor Protein-Tyrosine Kinases, Receptor, Ciliary Neurotrophic Factor, Receptor, trkA, Receptor, trkC, Receptors, Nerve Growth Factor, Vestibule, Labyrinth