Failure to maintain eye-specific segregation in nob, a mutant with abnormally patterned retinal activity.

Neuron
Jay DemasWilliam Guido

Abstract

Axon terminals from the two eyes initially overlap in the dorsal-lateral geniculate nucleus (dLGN) but subsequently refine to occupy nonoverlapping territories. Retinal activity is required to establish and maintain this segregation. We show that despite the presence of retinal activity, segregated projections desegregate when the structure of activity is altered. Early in development, spontaneous retinal activity in the no b-wave (nob) mouse is indistinguishable from that of wild-type mice, and eye-specific segregation proceeds normally. But, around eye-opening, spontaneous and visually evoked activity in nob retinas become abnormal, coincident with a failure to preserve precise eye-specific territories. Dark-rearing studies suggest that altered visual experience is not responsible. Transgenic rescue of the mutated protein (nyctalopin) within nob retinal interneurons, without rescuing expression in either retinal projection neurons or their postsynaptic targets in the dLGN, restores spontaneous retinal activity patterns and prevents desegregation. Thus, normally structured spontaneous retinal activity stabilizes newly refined retinogeniculate circuitry.

Citations

Jun 19, 2008·Annual Review of Neuroscience·Andrew D HubermanBarbara Chapman
Sep 25, 2009·Journal of Neurophysiology·Jokūbas ZiburkusWilliam Guido
Aug 26, 2014·PloS One·Jacob MenzlerGuenther Zeck
May 23, 2015·Journal of Neurophysiology·James T Pearson, Daniel Kerschensteiner
May 16, 2018·The European Journal of Neuroscience·Guela SokhadzeWilliam Guido
Jan 21, 2009·The Journal of Physiology·Anand R ChandrasekaranMichael C Crair
Jun 17, 2008·The Journal of Physiology·William Guido
Jun 4, 2015·Proceedings of the National Academy of Sciences of the United States of America·Samuel FailorHwai-Jong Cheng
Oct 27, 2015·Frontiers in Cellular Neuroscience·Florentina Soto, Daniel Kerschensteiner
Sep 23, 2016·Frontiers in Neural Circuits·Alexandra H Leighton, Christian Lohmann
Oct 3, 2017·Visual Neuroscience·Daniel Kerschensteiner, William Guido
Aug 10, 2007·Journal of Neurophysiology·Timothy A JonesBen Bonham
Mar 21, 2012·The Journal of Comparative Neurology·Siting WangAlev Erisir
Dec 20, 2011·Nature Neuroscience·Jiayi ZhangMichael C Crair
Jul 26, 2008·The Journal of Physiology·Maureen A McCall, Ronald G Gregg
Feb 24, 2016·Frontiers in Cellular Neuroscience·Günther Zeck
Nov 28, 2013·The Neuroscientist : a Review Journal Bringing Neurobiology, Neurology and Psychiatry·Daniel Kerschensteiner
Jun 1, 2016·Frontiers in Neural Circuits·Daniel Kerschensteiner
Oct 3, 2017·Visual Neuroscience·Aboozar MonavarfeshaniMichael A Fox
Dec 30, 2009·The Anatomical Record : Advances in Integrative Anatomy and Evolutionary Biology·Colenso M SpeerBarbara Chapman
Aug 17, 2016·Autism Research : Official Journal of the International Society for Autism Research·Ning ChengJong M Rho
Mar 14, 2008·Development, Growth & Differentiation·Kentaro Abe
Jul 25, 2021·International Journal of Molecular Sciences·Shermaine W Y LowShyam S Chaurasia
Oct 7, 2009·Cell·Jason W TriplettDavid A Feldheim
Jul 9, 2013·Neuron·Alejandro Akrouh, Daniel Kerschensteiner

❮ Previous
Next ❯

Related Concepts

Related Feeds

Ataxia telangiectasia

Ataxia telangiectasia is a rare neurodegenerative diseases caused by defects in the ATM gene, which is involved in DNA damage recognition and repair pathways. Here is the latest research on this autosomal recessive disease.

Ataxia telangiectasia (MDS)

Ataxia telangiectasia is a rare neurodegenerative diseases caused by defects in the ATM gene, which is involved in DNA damage recognition and repair pathways. Here is the latest research on this autosomal recessive disease.

Brain developing: Influences & Outcomes

This feed focuses on influences that affect the developing brain including genetics, fetal development, prenatal care, and gene-environment interactions. Here is the latest research in this field.