Elimination of glutamatergic transmission from Hb9 interneurons does not impact treadmill locomotion

• Published in: Scientific reports Vol. 11; no. 1; pp. 16008 - 17
• Main Authors: Koronfel, Lina M., Kanning, Kevin C., Alcos, Angelita, Henderson, Christopher E., Brownstone, Robert M.
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 06.08.2021; Nature Publishing Group; Nature Portfolio
• Subjects: 631/378; 631/443; Animal behavior; Animals; Cre recombinase; Female; Gait; Glutamatergic transmission; Glutamates - metabolism; Glutamic acid transporter; Homeobox; Homeodomain Proteins - physiology; Humanities and Social Sciences; Interneurons; Interneurons - physiology; Locomotion; Locomotor activity; Male; Mice; Mice, Transgenic; Motor neurons; multidisciplinary; Neural networks; Neurotransmission; Physical Conditioning, Animal; Science; Science (multidisciplinary); Spinal cord; Synapses - physiology; Synaptic Transmission; Transcription Factors - physiology; Vesicular Glutamate Transport Protein 2 - genetics; Vesicular Glutamate Transport Protein 2 - metabolism
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-021-95143-y

The spinal cord contains neural circuits that can produce the rhythm and pattern of locomotor activity. It has previously been postulated that a population of glutamatergic neurons, termed Hb9 interneurons, contributes to locomotor rhythmogenesis. These neurons were identified by their expression of the homeobox gene, Hb9, which is also expressed in motor neurons. We developed a mouse line in which Cre recombinase activity is inducible in neurons expressing Hb9. We then used this line to eliminate vesicular glutamate transporter 2 from Hb9 interneurons, and found that there were no deficits in treadmill locomotion. We conclude that glutamatergic neurotransmission by Hb9 interneurons is not required for locomotor behaviour. The role of these neurons in neural circuits remains elusive.