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Journal of Neuroscience, Vol 14, 4674-4683, Copyright © 1994 by Society for Neuroscience
Selective coexpression of insulin receptor-related receptor (IRR) and TRK in NGF-sensitive neurons
RR Reinhardt, E Chin, B Zhang, RA Roth and CA Bondy
Developmental Endocrinology Branch, NICHD, NIH, Bethesda, Maryland 20892.
The insulin receptor-related receptor (IRR) has recently been identified as
a member of the insulin receptor tyrosine kinase family; however, its
endogenous ligand and biological function are still unknown. In contrast to
the very widespread pattern of expression of the homologous insulin and
IGF-I receptors, IRR demonstrates a very restricted cellular distribution.
Using in situ hybridization and immunohistochemistry, we now show that the
expression of this receptor is selectively concentrated in a subset of
neurons where its appearance is closely associated with that of the NGF
receptor TRK. IRR and TRK demonstrate synchronized patterns of coexpression
in neural crest- derived sensory and sympathetic neurons and in non-neural
crest basal forebrain and striatal neurons. Both appear early in the
embryonic development of dorsal root and trigeminal neurons and somewhat
later, near the time of birth, in sympathetic neurons. Expression of both
IRR and TRK appears perinatally in basal forebrain neurons, reaching
maximal levels about postnatal day 20. This association is highly
selective, since TRK mRNA is not detected anywhere in the developing
nervous system in the absence of coordinate IRR expression, and the same is
true for IRR expression with respect to TRK. In the adult rat, the majority
of TRK-positive sensory neurons still express IRR mRNA, and coexpression in
sympathetic and forebrain neurons continues without evidence of diminution.
These findings are consistent with a functional linkage of the IRR and TRK
receptors in NGF-sensitive neurons.
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