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Pax6−/− Mice have a Cell Non‐Autonomous Defect in Non‐Radial Interneuron Migration
Author(s) -
Gopal Pallavi P,
Golden Jeffrey A
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a75-a
Subject(s) - ganglionic eminence , neocortex , pax6 , biology , interneuron , neuroscience , inhibitory postsynaptic potential , forebrain , excitatory postsynaptic potential , subventricular zone , embryonic stem cell , rostral migratory stream , anatomy , microbiology and biotechnology , progenitor cell , transcription factor , central nervous system , stem cell , gabaergic , genetics , gene
The mammalian neocortex is comprised of neuronal subtypes that can be classified as interneurons and projection neurons. These neuronal populations are derived from distinct progenitor zones: excitatory neurons from the cortical ventricular zone and interneurons from the ganglionic eminence (GE). These separate origins necessitate distinct pathways of migration. Using mouse genetics combined with embryonic forebrain slice culture assays, we sought to identify substrates and/or guidance molecules for non‐radial cell migration (NRCM). Mice carrying a mutation in Pax6 ( Small eye, Sey −/ − ), a paired domain transcription factor, are reported to have increased numbers of cortical inhibitory interneurons, suggesting Pax6 play a repressive role in guiding NRCM and/or specifying interneurons. Unexpectedly, we found a cell non‐autonomous reduction in the distance Sey −/ − neurons migrated. In contrast, no difference in the number of non‐radially migrating GE cells was observed in Sey −/ − mice. Our data indicate the increased numbers of interneurons observed in Sey −/ − do not result from an increased rate or number of non‐radially migrating cells; instead, loss of Pax6 results in the ectopic specification of interneurons in the cortical ventricular zone.