Abstract:
:The phenotype of neurotrophin-3 (NT-3) null mutant mice is characterized by sensory ataxia and early postnatal death. Previous analysis revealed a severe depletion of peripheral sensory, sympathetic and parasympathetic neurons. Most of the deficits are established early during embryonic development. Whereas absence of proprioceptive afferents can explain the sensory ataxia, the reasons for early postnatal death are unclear. To circumvent the limitations imposed by early mortality of null mutants we generated mouse line expressing NT-3 transgenes driven by the platelet-derived growth factor β-chain (PDGF-β) promoter, which is known to be active in neurons and mesenchyme derivatives. Mice carrying one or two PDGF-NT3 transgenes on a background null for wildtype NT-3 were generated by crossing with an NT-3 null strain. Although still ataxic, mice from this cross could survive for periods longer than a year. Histological analysis revealed a limited rescue of muscle spindles and parvalbumin immunoreactive sensory neurons.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Barski JJ,Helbig C,Meyer Mdoi
10.1016/j.neulet.2011.06.063subject
Has Abstractpub_date
2011-09-01 00:00:00pages
179-84issue
3eissn
0304-3940issn
1872-7972pii
S0304-3940(11)01057-3journal_volume
501pub_type
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