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Severe sensory and sympathetic deficits in mice lacking neurotrophin-3
Severe sensory and sympathetic deficits in mice lacking neurotrophin-3.
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During development, neurotrophins help shape the nervous system by regulating neuronal survival and differentiation. Neurotrophin-3 (refs 1-5) is the most abundant neurotrophin during early development. Neurons responsive to neurotrophin-3 in vitro include primary sensory, sympathetic, motor, enteric, locus coeruleus, hippocampal and cerebellar neurons (ref. 9 for example). Here we report that mice lacking neurotrophin-3 have severe deficits in sensory and sympathetic populations. These mice lack muscle spindles and show abnormal limb positions. In contrast, motor neurons, the enteric nervous system, and the major anatomical regions of the central nervous system seem to develop normally. Comparisons with mutants deficient in other neurotrophins or their receptors indicate that some neurons require more than one neurotrophin during embryogenesis and suggest that neurotrophin-3 functions by binding receptors in addition to its primary receptor trkC (ref. 16). In particular, neurotrophin-3 is essential for survival of sympathetic and sensory neurons that later become dependent on nerve growth factor or brain-derived neurotrophic factor.
Fariñas I, Jones KR, Backus C, Wang XY, Reichardt LF
Nature
1994-06-23 00:00
369
6482
658-61
Animals,Animals, Newborn,Cell Count,Mice,Muscles,Nerve Growth Factors,Nervous System Diseases,Neurons, Afferent,Neurotrophin 3,Receptor Protein-Tyrosine Kinases,Receptor, trkC,Receptors, Growth Factor,Sympathetic Nervous System,Nerve Growth Factors,Neurotrophin 3,Receptors, Growth Factor,Receptor Protein-Tyrosine Kinases,Receptor, trkC
Department of Physiology, University of California School of Medicine, San Francisco 94143-0724
Nature
0028-0836
10.1038/369658a0
601
True
8208292
