Back to Search
Start Over
Genetic ablation of V2a ipsilateral interneurons disrupts left-right locomotor coordination in mammalian spinal cord.
Genetic ablation of V2a ipsilateral interneurons disrupts left-right locomotor coordination in mammalian spinal cord.
- Source :
-
Neuron [Neuron] 2008 Oct 09; Vol. 60 (1), pp. 70-83. - Publication Year :
- 2008
-
Abstract
- The initiation and coordination of activity in limb muscles are the main functions of neural circuits that control locomotion. Commissural neurons connect locomotor circuits on the two sides of the spinal cord, and represent the known neural substrate for left-right coordination. Here we demonstrate that a group of ipsilateral interneurons, V2a interneurons, plays an essential role in the control of left-right alternation. In the absence of V2a interneurons, the spinal cord fails to exhibit consistent left-right alternation. Locomotor burst activity shows increased variability, but flexor-extensor coordination is unaffected. Anatomical tracing studies reveal a direct excitatory input of V2a interneurons onto commissural interneurons, including a set of molecularly defined V0 neurons that drive left-right alternation. Our findings imply that the neural substrate for left-right coordination consists of at least two components; commissural neurons and a class of ipsilateral interneurons that activate commissural pathways.
- Subjects :
- Afferent Pathways physiology
Animals
Electric Stimulation methods
Female
Functional Laterality genetics
Homeodomain Proteins genetics
Male
Mice
Mice, Inbred C57BL
Mice, Transgenic
Motor Activity genetics
Psychomotor Performance physiology
Transcription Factors deficiency
Transcription Factors genetics
Functional Laterality physiology
Gene Deletion
Interneurons physiology
Motor Activity physiology
Recombination, Genetic
Spinal Cord physiology
Subjects
Details
- Language :
- English
- ISSN :
- 1097-4199
- Volume :
- 60
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Neuron
- Publication Type :
- Academic Journal
- Accession number :
- 18940589
- Full Text :
- https://doi.org/10.1016/j.neuron.2008.08.009