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Spinal Hb9::Cre-derived excitatory interneurons contribute to rhythm generation in the mouse
Journal article   Open access   Peer reviewed

Spinal Hb9::Cre-derived excitatory interneurons contribute to rhythm generation in the mouse

Vanessa Caldeira, Kimberly J Dougherty, Lotta Borgius and Ole Kiehn
Scientific reports, v 7(1), pp 41369-41369
27 Jan 2017
PMID: 28128321
url
https://doi.org/10.1038/srep41369View
Published, Version of Record (VoR)CC BY V4.0 Open

Abstract

Animals Evoked Potentials Gene Silencing Glutamates - metabolism Homeodomain Proteins - metabolism Integrases - metabolism Interneurons - metabolism Lumbar Vertebrae - metabolism Mice Mice, Transgenic Motor Activity - physiology Motor Neurons - metabolism Spinal Cord - metabolism Synapses - metabolism Synaptic Transmission Transcription Factors - metabolism Vesicular Glutamate Transport Protein 2 - metabolism
Rhythm generating neurons are thought to be ipsilaterally-projecting excitatory neurons in the thoracolumbar mammalian spinal cord. Recently, a subset of Shox2 interneurons (Shox2 non-V2a INs) was found to fulfill these criteria and make up a fraction of the rhythm-generating population. Here we use Hb9::Cre mice to genetically manipulate Hb9::Cre-derived excitatory interneurons (INs) in order to determine the role of these INs in rhythm generation. We demonstrate that this line captures a consistent population of spinal INs which is mixed with respect to neurotransmitter phenotype and progenitor domain, but does not overlap with the Shox2 non-V2a population. We also show that Hb9::Cre-derived INs include the comparatively small medial population of INs which continues to express Hb9 postnatally. When excitatory neurotransmission is selectively blocked by deleting Vglut2 from Hb9::Cre-derived INs, there is no difference in left-right and/or flexor-extensor phasing between these cords and controls, suggesting that excitatory Hb9::Cre-derived INs do not affect pattern generation. In contrast, the frequencies of locomotor activity are significantly lower in cords from Hb9::Cre-Vglut2 mice than in cords from controls. Collectively, our findings indicate that excitatory Hb9::Cre-derived INs constitute a distinct population of neurons that participates in the rhythm generating kernel for spinal locomotion.

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