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The avian forebrain displays no lamination that corresponds to the mammalian neocortex, hence lamination does not seem to be a requirement for higher cognitive functions.
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Because there was no clear lamination from depths of 17.3 to 19.1 cm, we considered this part as temporarily bioturbated and interpolated the sedimentation rate (cm/year) based on the average varve thickness in other parts (2.5 ± 1.2 mm/year).
Dcx KO mice have no obvious lamination defects in the isocortex [11], [12].
This analysis revealed no obvious lamination defects in single Pafah1b1+/− or Vldlr−/− mice, whereas some layer abnormalities were observed in single Apoer2−/− mice, as previously reported [9], [25] (Fig. 5).
Perhaps surprisingly, no gross lamination abnormalities were observed.
Though Pten:Neurod6 mutants die around birth, no overt lamination defects were observed.
Cdc42 Neurod6 mutants also die shortly after birth, but again we observed no gross lamination defect in these mutant mice.
In sharp contrast, no cell lamination defects were observed in the CA1 region in all animals examined.
Histological examination of the developing retina in cep290 knockdown embryos revealed no gross lamination defects; however, functional analysis of vision revealed a reduction in visual behavior.
Similarly, the histological examination of retinas from cep290 MO-injected zebrafish revealed no gross lamination defects, yet the embryos had a statistically significant reduction in visual function.
No de-lamination of the strip was observed in any of the retrofitted beams.
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