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A novel form of migration of glial precursors
Author(s) -
Orentas Diana M.,
Miller Robert H.
Publication year - 1996
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/(sici)1098-1136(199601)16:1<27::aid-glia4>3.0.co;2-8
Subject(s) - biology , neuroglia , neuroscience , cognitive science , central nervous system , psychology
During development of the vertebrate central nervous system, many types of neural precursors originate in the ventricular zone of the central nervous system (CNS) and migrate through the neuropil to their final destination. In embryonic rat spinal cord, the ventral ventricular zone gives rise to neurons, astrocytes, and oligodendrocyte precursors. We have used a spinal cord stripe preparation to examine the migration of neural precursors from different regions of the spinal cord ventricular zone in vitro. Astrocyte and oligodendrocyte precursors, neurons, and neurites all emigrated from stripes of embryonic day 14 (E14) rat ventral spinal cord while only neurites emigrated in significant numbers from stripes of E14 dorsal spinal cord. The first wave of migrating cells from E14 ventral spinal cord stripes comprised a population of A2B5+ astrocyte precursors that exhibited a semicircular or ellipsoid morphology and showed an unusual form of lamellipodia‐based motility. These cells were highly motile, migrating at rates of approximately 20 μm/h. The cortical region of the rapidly translocating astrocyte precursors contained high levels of actin microfilaments oriented in a circumferential band, but few microtubules. In their morphology, cytoskeletal organization, and rapid translocation, this subpopulation of vertebrate CNS glial precursors more closely resemble epidermal keratocytes than other neural cells. The rapid translocation exhibited by A2B5+ astrocyte precursors may reflect a role in CNS wound healing and be responsible for the rapid spread of some forms of CNS glial tumors. © 1996 Wiley‐Liss, Inc.