Congenital Nystagmus Gene FRMD7 Is Necessary for Establishing a Neuronal Circuit Asymmetry for Direction Selectivity.
Fiche du document
- doi: 10.1016/j.neuron.2015.11.032
- issn: 0896-6273
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.neuron.2015.11.032
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/pmid/26711119
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/eissn/1097-4199
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_891621F3D8947
info:eu-repo/semantics/openAccess , Copying allowed only for non-profit organizations , https://serval.unil.ch/disclaimer
Citer ce document
K. Yonehara et al., « Congenital Nystagmus Gene FRMD7 Is Necessary for Establishing a Neuronal Circuit Asymmetry for Direction Selectivity. », Serveur académique Lausannois, ID : 10.1016/j.neuron.2015.11.032
Métriques
Partage / Export
Résumé
Neuronal circuit asymmetries are important components of brain circuits, but the molecular pathways leading to their establishment remain unknown. Here we found that the mutation of FRMD7, a gene that is defective in human congenital nystagmus, leads to the selective loss of the horizontal optokinetic reflex in mice, as it does in humans. This is accompanied by the selective loss of horizontal direction selectivity in retinal ganglion cells and the transition from asymmetric to symmetric inhibitory input to horizontal direction-selective ganglion cells. In wild-type retinas, we found FRMD7 specifically expressed in starburst amacrine cells, the interneuron type that provides asymmetric inhibition to direction-selective retinal ganglion cells. This work identifies FRMD7 as a key regulator in establishing a neuronal circuit asymmetry, and it suggests the involvement of a specific inhibitory neuron type in the pathophysiology of a neurological disease. VIDEO ABSTRACT.