Genetic absence of the vesicular inhibitory amino acid transporter differentially regulates respiratory and locomotor motor neuron development

Fogarty, Matthew J., Yanagawa, Yuchio, Obata, Kunihiko, Bellingham, Mark C. and Noakes, Peter G. (2013) Genetic absence of the vesicular inhibitory amino acid transporter differentially regulates respiratory and locomotor motor neuron development. Brain Structure and Function, Online First 1-16. doi:10.1007/s00429-013-0673-9

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Author Fogarty, Matthew J.
Yanagawa, Yuchio
Obata, Kunihiko
Bellingham, Mark C.
Noakes, Peter G.
Title Genetic absence of the vesicular inhibitory amino acid transporter differentially regulates respiratory and locomotor motor neuron development
Journal name Brain Structure and Function   Check publisher's open access policy
ISSN 1863-2653
1863-2661
Publication date 2013-11-26
Year available 2013
Sub-type Article (original research)
DOI 10.1007/s00429-013-0673-9
Volume Online First
Start page 1
End page 16
Total pages 16
Place of publication Heidelberg, Germany
Publisher Springer
Language eng
Formatted abstract
During mid to late embryonic development (E13 to birth in mice), the neuromotor system is refined by reducing motor neuron (MN) numbers and establishing nascent synaptic connections onto and by MNs. Concurrently, the response to GABAergic and glycinergic synaptic activity switches from postsynaptic excitation to inhibition. Our previous studies on mutant mice lacking glycinergic transmission or deficient in GABA suggests that altered MN activity levels during this developmental period differentially regulates MN survival and muscle innervation for respiratory and non-respiratory motor pools. To determine if combined loss of GABAergic and glycinergic transmission plays a similar or exaggerated role, we quantified MN number and muscle innervation in two respiratory (hypoglossal and phrenic) and two locomotor (brachial and lumbar) motor pools, in mice lacking vesicular inhibitory amino acid transporter, which display absent or severely impaired GABAergic and glycinergic neurotransmission. For respiratory MNs, we observed significant decreases in MN number (−20 % hypoglossal and −36 % phrenic) and diaphragm axonal branching (−60 %). By contrast, for non-respiratory brachial and lumbar MNs, we observed increases in MN number (+62 % brachial and +84 % lumbar) and axonal branching for innervated muscles (+123 % latissimus dorsi for brachial and +61 % gluteal for lumbar). These results show that combined absence of GABAergic and glycinergic neurotransmission causes distinct regional changes in MN number and muscle innervation, which are dependent upon the motor function of the specific motor pool.
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Queensland Brain Institute Publications
Official 2014 Collection
School of Biomedical Sciences Publications
 
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Created: Tue, 03 Dec 2013, 23:00:07 EST by Dr Mark Bellingham on behalf of School of Biomedical Sciences