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The Journal of Neuroscience, August 15, 1998, 18(16):6370-6377
Cyclin-Dependent Kinase 5-Deficient Mice Demonstrate Novel
Developmental Arrest in Cerebral Cortex
Edward C.
Gilmore1,
Toshio
Ohshima3, 4,
André M.
Goffinet5,
Ashok B.
Kulkarni4, and
Karl
Herrup1, 2
1 Department of Neuroscience, 2 Alzheimer
Research Laboratory, Case Western Reserve Medical School, Cleveland,
Ohio 44106, 3 Developmental and Metabolic Neurology,
National Institute of Neurological Disorders and Stroke,
4 Gene Targeting Research and Core Facility, National
Institute of Dental Research, National Institutes of Health, Bethesda,
Maryland 20892, and 5 Département de Physiologie,
FUNDP, B5000 Namur, Belgium
The cerebral cortex of mice with a targeted disruption in the gene
for cyclin-dependent kinase 5 (cdk5) is abnormal in its structure. Bromodeoxyuridine labeling reveals that the normal inside-out neurogenic gradient is inverted in the mutants; earlier born
neurons are most often found superficial to those born later. Despite
this, the early preplate layer separates correctly and neurons with a
normal, pyramidal morphology can be found between true marginal zone
and subplate. Consistent with their identity as layer VI
corticothalamic neurons, they can be labeled by DiI injections into
thalamus. The DiI injections also reveal that the trajectories of the
cdk5 / thalamocortical axons are
oblique and cut across the entire cortical plate, instead of being
oriented tangentially in the subcortical white matter. We propose a
model in which the cdk5/ defect
blocks cortical development at a heretofore undescribed intermediate
stage, after the splitting of the preplate, but before the migration of
the full complement of cortical neurons.
Key words:
neuronal migration; cdk5; reeler; cerebral
cortical development; neuronal morphology; BrdU
Copyright © 1998 Society for Neuroscience 0270-6474/98/18166370-08$05.00/0
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