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Neuronal deficits, not involving motor neurons, in mice lacking BDNF and/or NT4.

Nerve growth factor and other neurotrophins signal to neurons through the Trk family of receptor tyrosine kinases. TrkB is relatively promiscuous in vitro, acting as a receptor for brain-derived neurotrophic factor (BDNF), neurotrophin-4 (NT4) and, to a lesser extent, NT3 (refs 3-5). Mice lacking TrkB show a more severe phenotype than mice lacking BDNF, suggesting that TrkB may act as a receptor for additional ligands in vivo. To explore this possibility, we generated mice lacking NT4 or BDNF as well as mice lacking both neurotrophins. Unlike mice lacking other Trks or neurotrophins, NT4-deficient mice are long-lived and show no obvious neurological defects. Analysis of mutant phenotypes revealed distinct neuronal populations with different neurotrophin requirements. Thus vestibular and trigeminal sensory neurons require BDNF but not NT4, whereas nodose-petrosal sensory neurons require both BDNF and NT4. Motor neurons, whose numbers are drastically reduced in mice lacking TrkB, are not affected even in mice lacking both BDNF and NT4. These results suggest that another ligand, perhaps NT3, does indeed act on TrkB in vivo.

Pubmed ID: 7746324

Authors

  • Conover JC
  • Erickson JT
  • Katz DM
  • Bianchi LM
  • Poueymirou WT
  • McClain J
  • Pan L
  • Helgren M
  • Ip NY
  • Boland P

Journal

Nature

Publication Data

May 18, 1995

Associated Grants

None

Mesh Terms

  • Animals
  • Brain-Derived Neurotrophic Factor
  • Mice
  • Mice, Inbred BALB C
  • Motor Neurons
  • Mutagenesis
  • Nerve Growth Factors
  • Nerve Tissue Proteins
  • Nervous System Diseases
  • Neurons, Afferent
  • Receptor, Ciliary Neurotrophic Factor
  • Receptors, Nerve Growth Factor