Netrin-4 regulates thalamocortical axon branching in an activity-dependent fashion.
Proc Natl Acad Sci U S A
; 111(42): 15226-31, 2014 Oct 21.
Article
em En
| MEDLINE
| ID: mdl-25288737
ABSTRACT
Axon branching is remodeled by sensory-evoked and spontaneous neuronal activity. However, the underlying molecular mechanism is largely unknown. Here, we demonstrate that the netrin family member netrin-4 (NTN4) contributes to activity-dependent thalamocortical (TC) axon branching. In the postnatal developmental stages of rodents, ntn4 expression was abundant in and around the TC recipient layers of sensory cortices. Neuronal activity dramatically altered the ntn4 expression level in the cortex in vitro and in vivo. TC axon branching was promoted by exogenous NTN4 and suppressed by depletion of the endogenous protein. Moreover, unc-5 homolog B (Unc5B), which strongly bound to NTN4, was expressed in the sensory thalamus, and knockdown of Unc5B in thalamic cells markedly reduced TC axon branching. These results suggest that NTN4 acts as a positive regulator for TC axon branching through activity-dependent expression.
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MEDLINE
Assunto principal:
Axônios
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Tálamo
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Córtex Cerebral
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Receptores de Superfície Celular
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Fatores de Crescimento Neural
Idioma:
En
Revista:
Proc Natl Acad Sci U S A
Ano de publicação:
2014
Tipo de documento:
Article