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Journal of Neuroscience, Vol 16, 2283-2293, Copyright © 1996 by Society for Neuroscience
Role of neuron-glial junctional domain proteins in the maintenance and termination of neuronal migration across the embryonic cerebral wall
ES Anton, RS Cameron and P Rakic
Section of Neurobiology, Yale University School of Medicine, New Haven, Connecticut 06510-8001, USA.
To identify glial membrane proteins that contribute to the process of
neuronal migration in the developing brain, we developed a polyclonal
antiserum (D4) and a monoclonal antibody (NJPA1: neuron-glial junctional
polypeptide antibody) that recognize membrane proteins localized to the
plasmalemmal junction between migrating neurons and adjacent radial glial
fibers (Cameron and Rakic, 1994). Here, we show that in the developing
cerebral cortex, immunoreactivity for these junctional polypeptides is
present throughout the neuronal migratory pathway but becomes minimal or
absent where radial glial cell processes enter the marginal zone region,
the barrier at which newly arrived neurons normally stop their migration
and detach from their glial fiber substrate. We thus tested, using imprints
of embryonic cerebral wall and slice preparations, whether the junctional
membrane proteins detected by our antibodies contribute to the regulation
of neuronal migration in the cerebral cortex. The rate of neuronal
migration on glial cell substrates was reduced significantly in the
presence of D4 or NJPA1 antibodies. Antibody exposure typically led to the
withdrawal of leading processes, changes in microtubular organization and,
in some instances, to detachment of neurons from their glial cell
substrates. These results suggest that the polypeptides recognized by the
D4 and NJPA1 antibodies are essential for the maintenance of normal
neuronal migration. Dismantling of neuron-glial cell junctional domains
formed by these membrane proteins may underlie neuronal cell detachment
from glial migratory substrates at the interface between cortical plate and
marginal zone in the developing cerebral wall.
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