|  Help  |  About  |  Contact Us

Publication : EphA signaling impacts development of topographic connectivity in auditory corticofugal systems.

First Author  Torii M Year  2013
Journal  Cereb Cortex Volume  23
Issue  4 Pages  775-85
PubMed ID  22490549 Mgi Jnum  J:208463
Mgi Id  MGI:5563324 Doi  10.1093/cercor/bhs066
Citation  Torii M, et al. (2013) EphA signaling impacts development of topographic connectivity in auditory corticofugal systems. Cereb Cortex 23(4):775-85
abstractText  Auditory stimulus representations are dynamically maintained by ascending and descending projections linking the auditory cortex (Actx), medial geniculate body (MGB), and inferior colliculus. Although the extent and topographic specificity of descending auditory corticofugal projections can equal or surpass that of ascending corticopetal projections, little is known about the molecular mechanisms that guide their development. Here, we used in utero gene electroporation to examine the role of EphA receptor signaling in the development of corticothalamic (CT) and corticocollicular connections. Early in postnatal development, CT axons were restricted to a deep dorsal zone (DDZ) within the MGB that expressed low levels of the ephrin-A ligand. By hearing onset, CT axons had innervated surrounding regions of MGB in control-electroporated mice but remained fixed within the DDZ in mice overexpressing EphA7. In vivo neurophysiological recordings demonstrated a corresponding reduction in spontaneous firing rate, but no changes in sound-evoked responsiveness within MGB regions deprived of CT innervation. Structural and functional CT disruption occurred without gross alterations in thalamocortical connectivity. These data demonstrate a potential role for EphA/ephrin-A signaling in the initial guidance of corticofugal axons and suggest that "genetic rewiring" may represent a useful functional tool to alter cortical feedback without silencing Actx.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

1 Bio Entities

Trail: Publication

0 Expression