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Mice lacking NT‐3, and its receptor TrkC, exhibit profound deficiencies in CNS glial cells
Author(s) -
Kahn M.A.,
Kumar S.,
Liebl D.,
Chang R.,
Parada L.F.,
De Vellis J.
Publication year - 1999
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(199904)26:2<153::aid-glia6>3.0.co;2-z
Subject(s) - biology , subventricular zone , knockout mouse , tropomyosin receptor kinase c , oligodendrocyte , neuroglia , progenitor cell , neurotrophin 3 , microbiology and biotechnology , microglia , neuroscience , stem cell , immunology , receptor , myelin , central nervous system , brain derived neurotrophic factor , neurotrophic factors , growth factor , platelet derived growth factor receptor , inflammation , genetics
Neurotrophin‐3 (NT‐3) and its receptor TrkC are known to be important for neuronal survival. More recently, NT‐3 has been implicated as playing a role in oligodendrocyte (OL) proliferation and survival in vitro. Examination of NT‐3 and TrkC knockout mice revealed a reduction in NT‐3‐dependent neurons. To date, no study has examined alterations in glial cell populations in these knockout mice. In this report, we demonstrate a decline in OL progenitor cell numbers within the CNS of NT‐3 and TrkC knockout mice. We also observed that immature and mature OL‐specific markers were attenuated in the NT‐3 and TrkC knockout animals. Deficiencies in other CNS glial cells, including astrocytes and ameboid microglia, were also observed. The subventricular zone (SVZ), a highly proliferative region for progenitor glial cells, was reduced in size. Furthermore, a nuclear‐specific stain revealed a decline in the numbers of pyknotic nuclei in and around the SVZ of the knockout mice. These data will support an in vivo NT‐3‐dependent mechanism for the normal development of CNS glial cells. GLIA 26:153–165, 1999. © 1999 Wiley‐Liss, Inc.