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

Title:
Neuronal deficits, not involving motor neurons, in mice lacking BDNF and/or NT4
Authors:
Conover, J. C.; Erickson, J. T.; Katz, D. M.; Bianchi, Lynne M.; Poueymirou, W. T.; McClain, J.; Pan, L.; Helgren, M.; Ip, N. Y.; Boland, P.; Friedman, B.; Wiegand, Stanley; Vejsada, R.; Kato, A. C.; Dechiara, T. M.; Yancopoulos, George D.
Abstract:
NERVE growth factor and other neurotrophins signal to neurons through the Trk family of receptor tyrosine kinases1–6. 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 TrkB7 show a more severe phenotype than mice lacking BDNF8,9, 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 Trks7,10,11 or neurotrophins8,9,12–14, 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 trigemi-nal 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.
Citation:
Conover, J.C., J.T. Erickson, D.M. Katz, L.M. Bianchi, et al. 1995. "Neuronal deficits, not involving motor neurons, in mice lacking BDNF and/or NT4." Nature 375: 235-238.
Publisher:
Nature Publishing Group
DATE ISSUED:
1995-05-18
Department:
Neuroscience
Type:
article
PUBLISHED VERSION:
10.1038/375235a0
PERMANENT LINK:
http://hdl.handle.net/11282/309750

Full metadata record

DC FieldValue Language
dc.contributor.authorConover, J. C.en_US
dc.contributor.authorErickson, J. T.en_US
dc.contributor.authorKatz, D. M.en_US
dc.contributor.authorBianchi, Lynne M.en_US
dc.contributor.authorPoueymirou, W. T.en_US
dc.contributor.authorMcClain, J.en_US
dc.contributor.authorPan, L.en_US
dc.contributor.authorHelgren, M.en_US
dc.contributor.authorIp, N. Y.en_US
dc.contributor.authorBoland, P.en_US
dc.contributor.authorFriedman, B.en_US
dc.contributor.authorWiegand, Stanleyen_US
dc.contributor.authorVejsada, R.en_US
dc.contributor.authorKato, A. C.en_US
dc.contributor.authorDechiara, T. M.en_US
dc.contributor.authorYancopoulos, George D.en_US
dc.date.accessioned2013-12-23T16:17:02Zen
dc.date.available2013-12-23T16:17:02Zen
dc.date.issued1995-05-18en
dc.identifier.citationConover, J.C., J.T. Erickson, D.M. Katz, L.M. Bianchi, et al. 1995. "Neuronal deficits, not involving motor neurons, in mice lacking BDNF and/or NT4." Nature 375: 235-238.en_US
dc.identifier.issn0028-0836en_US
dc.identifier.urihttp://hdl.handle.net/11282/309750en
dc.description.abstractNERVE growth factor and other neurotrophins signal to neurons through the Trk family of receptor tyrosine kinases1–6. 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 TrkB7 show a more severe phenotype than mice lacking BDNF8,9, 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 Trks7,10,11 or neurotrophins8,9,12–14, 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 trigemi-nal 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.en_US
dc.language.isoen_USen_US
dc.publisherNature Publishing Groupen_US
dc.identifier.doi10.1038/375235a0en
dc.subject.departmentNeuroscienceen_US
dc.titleNeuronal deficits, not involving motor neurons, in mice lacking BDNF and/or NT4en_US
dc.typearticleen_US
dc.identifier.journalNatureen_US
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