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   <subfield code="a">The disorganized visual cortex in reelin-deficient mice is functional and allows for enhanced plasticity</subfield>
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   <subfield code="c">[Justyna Pielecka-Fortuna, Robin Wagener, Ann-Kristin Martens, Bianka Goetze, Karl-Friedrich Schmidt, Jochen Staiger, Siegrid Löwel]</subfield>
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   <subfield code="a">A hallmark of neocortical circuits is the segregation of processing streams into six distinct layers. The importance of this layered organization for cortical processing and plasticity is little understood. We investigated the structure, function and plasticity of primary visual cortex (V1) of adult mice deficient for the glycoprotein reelin and their wild-type littermates. In V1 of rl−/− mice, cells with different laminar fates are present at all cortical depths. Surprisingly, the (vertically) disorganized cortex maintains a precise retinotopic (horizontal) organization. Rl−/− mice have normal basic visual capabilities, but are compromised in more challenging perceptual tasks, such as orientation discrimination. Additionally, rl−/− animals learn and memorize a visual task as well as their wild-type littermates. Interestingly, reelin deficiency enhances visual cortical plasticity: juvenile-like ocular dominance plasticity is preserved into late adulthood. The present data offer an important insight into the capabilities of a disorganized cortical system to maintain basic functional properties.</subfield>
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