Abstract
The external globus pallidus (GPe) is an essential component of the basal ganglia, a group of subcortical nuclei that are involved in control of action. Changes in the firing of GPe neurons are associated with both passive and active body movements. Aberrant activity of GPe neurons has been linked to motor symptoms of a variety of movement disorders, such as Parkinson's Disease, Huntington's disease and dystonia. Recent studies have helped delineate functionally distinct subtypes of GABAergic GPe projection neurons. However, not much is known about specific molecular mechanisms underlying the development of GPe neuronal subtypes. We show that the transcriptional regulator Lmo3 is required for the development of medial ganglionic eminence derived Nkx2.1+ and PV+ GPe neurons, but not lateral ganglionic eminence derived FoxP2+ neurons. As a consequence of the reduction in PV+ neurons, Lmo3-null mice have a reduced GPe input to the subthalamic nucleus.
Original language | English (US) |
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Pages (from-to) | 10-24 |
Number of pages | 15 |
Journal | Developmental Biology |
Volume | 503 |
DOIs | |
State | Published - Nov 2023 |
Funding
This work was supported by The National Institutes of Health EY026614 to L.G., the Research to Prevent Blindness challenge grant to the Department of Ophthalmology at the University of Rochester , NIMH R01 MH081880 to J.L.R. and NIH R01 NS069777 to C.S.C.
Keywords
- Basal ganglia
- GPe
- Lmo3
- Medial ganglionic eminence
- Parvalbumin
ASJC Scopus subject areas
- Molecular Biology
- Developmental Biology
- Cell Biology