mortality/aging
• all homozygotes die at perinatal stages
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nervous system
• corpus callosum and hippocampal commissure are stunted at midline
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• at E18.5, callosal projections in mutants fail to show decussation in most fetuses
• non-crossing commissural fibers have an abnormal defasciculated appearance
• at all levels, callosal projections form aberrantly oriented Probst bundles
• mutants fail to show segregation of anterior versus posterior projections
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• failure of hippocampal commissure to cross midline is observed and ventrally oriented ectopic thick bundles are seen
• all hippocampal fibers form a thick bundle together with the fornix which shows aberrant growth into the septal region
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• number of anterior limb branches of the anterior commissure (AC) in the olfactory cortex is increased
• anterior and posterior branching are abnormally positioned dorsoventrally; innervation of anteromedial cortex by these branches is through numerous tracts
• some AC fascicles show aberrant connections with hippocampal commissure
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• embryos present a significantly extended length of medial cortex compared with dorsoventral length of the telencephalon
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• embryos present a ventrally extended cingulate cortex
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• cultured hippocampal neurons from mutants have no protrusions or a slightly elongated process after 12 hours
• when normal neurons show a symmetrical distribution of neurites, mutant neurons have no processes or abnormal neurites that tended to curl up on themselves
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• all major forebrain commissures have guidance abnormalities along anterior-posterior and dorsoventral axesin mutants
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• cultured neurons display numerous short filopodial extensions and growth cone-like structures around the cell body and neurites; axons roll up in an abnormal fashion
• Map1b protein levels in growing axons are decreased significantly
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cellular
• all major forebrain commissures have guidance abnormalities along anterior-posterior and dorsoventral axesin mutants
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