1. Molecular Neurobiology Laboratory and
2. System Neurobiology Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA
3. Mammalian Locomotor Laboratory, Department of Neuroscience, The Karolinska Institute, Retzius vag 8, Stockholm 17177, Sweden
4. Centre for Molecular Neurobiology, University of Hamburg, Hamburg 20251, Germany
5. †Present address: Department of Developmental Genetics, The Skirball Institute, New York University, New York, New York 10016, USA
6. *These authors contributed equally to this work

Correspondence to: Martyn Goulding¹ Correspondence and requests for materials should be addressed to M.G. (Email: goulding@salk.edu).

Abstract

The neuronal networks that generate vertebrate movements such as walking and swimming are embedded in the spinal cord^{1, 2, 3}. These networks, which are referred to as central pattern generators (CPGs), are ideal systems for determining how ensembles of neurons generate simple behavioural outputs. In spite of efforts to address the organization of the locomotor CPG in walking animals^{2, 4, 5, 6}, little is known about the identity and function of the spinal interneuron cell types that contribute to these locomotor networks. Here we use four complementary genetic approaches to directly address the function of mouse V1 neurons, a class of local circuit inhibitory interneurons that selectively express the transcription factor Engrailed1. Our results show that V1 neurons shape motor outputs during locomotion and are required for generating 'fast' motor bursting. These findings outline an important role for inhibition in regulating the frequency of the locomotor CPG rhythm, and also suggest that V1 neurons may have an evolutionarily conserved role in controlling the speed of vertebrate locomotor movements.

1. Molecular Neurobiology Laboratory and
2. System Neurobiology Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA
3. Mammalian Locomotor Laboratory, Department of Neuroscience, The Karolinska Institute, Retzius vag 8, Stockholm 17177, Sweden
4. Centre for Molecular Neurobiology, University of Hamburg, Hamburg 20251, Germany
5. †Present address: Department of Developmental Genetics, The Skirball Institute, New York University, New York, New York 10016, USA
6. *These authors contributed equally to this work

Correspondence to: Martyn Goulding¹ Correspondence and requests for materials should be addressed to M.G. (Email: goulding@salk.edu).

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