Journal
JOURNAL OF COMPARATIVE NEUROLOGY
Volume 510, Issue 1, Pages 79-99Publisher
WILEY
DOI: 10.1002/cne.21772
Keywords
Lhx6; Dlx; GABAergic; interneuron; NPY
Categories
Funding
- Nina Ireland
- Larry L. Hillblom Foundation
- National Institute of Mental Health [RO1 MH49428-01, K05 MH065670]
- Swiss National Science Foundation [PA00A-117463, PBGEA-112882]
- Intramural Research Program of the National Institute of Child Health and Human Development
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT [Z01HD000071] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF MENTAL HEALTH [K05MH065670, R01MH081880, R37MH049428, R01MH049428] Funding Source: NIH RePORTER
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Here we analyze the role of the Lhx6 lim-homeobox transcription factor in regulating the development of subsets of neocortical, hippocampal, and striatal interneurons. An Lhx6 loss-of-function allele, which expresses placental alkaline phosphatase (PLAP), allowed analysis of the development and fate of Lhx6-expressing interneurons in mice lacking this homeobox transcription factor. There are Lhx6(+)-;Dlx(+) and Lhx6(-);Dlx(+) subtypes of tangentially migrating interneurons. Most interneurons in Lhx6(PLAP/PLAP) mutants migrate to the cortex, although less efficiently, and exhibit defects in populating the marginal zone and superficial parts of the neocortical plate. By contrast, migration to superficial parts of the hippocampus is not seriously affected. Furthermore, whereas parvalbumin(+) and somatostatin(+) interneurons do not differentiate, NPY+ interneurons are present; we suggest that these NPY+ interneurons are derived from the Lhx6(-);Dlx(+) subtype. Striatal interneurons show deficits distinct from pallial interneurons, including a reduction in the NPY+ subtype. We provide evidence that Lhx6 mediates these effects through promoting expression of receptors that regulate interneuron migration (ErbB4, CXCR4, and CXCR7), and through promoting the expression of transcription factors either known (Arx) or implicated (bMaf, Cux2, and NPAS1) in controlling interneuron development.
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