TY - JOUR T1 - NMNAT Proteins that Limit Wallerian Degeneration Also Regulate Critical Period Plasticity in the Visual Cortex JF - eneuro JO - eNeuro DO - 10.1523/ENEURO.0277-18.2018 VL - 6 IS - 1 SP - ENEURO.0277-18.2018 AU - Mariska van Lier AU - Laura Smit-Rigter AU - Roos Krimpenfort AU - M. Hadi Saiepour AU - Emma Ruimschotel AU - Willem Kamphuis AU - J. Alexander Heimel AU - Christiaan N. Levelt Y1 - 2019/01/01 UR - http://www.eneuro.org/content/6/1/ENEURO.0277-18.2018.abstract N2 - Many brain regions go through critical periods of development during which plasticity is enhanced. These critical periods are associated with extensive growth and retraction of thalamocortical and intracortical axons. Here, we investigated whether a signaling pathway that is central in Wallerian axon degeneration also regulates critical period plasticity in the primary visual cortex (V1). Wallerian degeneration is characterized by rapid disintegration of axons once they are separated from the cell body. This degenerative process is initiated by reduced presence of cytoplasmic nicotinamide mononucleotide adenylyltransferases (NMNATs) and is strongly delayed in mice overexpressing cytoplasmic NMNAT proteins, such as WldS mutant mice producing a UBE4b-NMNAT1 fusion protein or NMNAT3 transgenic mice. Here, we provide evidence that in WldS mice and NMNAT3 transgenic mice, ocular dominance (OD) plasticity in the developing visual cortex is reduced. This deficit is only observed during the second half of the critical period. Additionally, we detect an early increase of visual acuity in the V1 of WldS mice. We do not find evidence for Wallerian degeneration occurring during OD plasticity. Our findings suggest that NMNATs do not only regulate Wallerian degeneration during pathological conditions but also control cellular events that mediate critical period plasticity during the physiological development of the cortex. ER -