Abstract
AbstractMovement and posture depend on sensory feedback that is regulated by specialized GABAergic neurons (GAD2+) that form axo-axonic contacts onto myelinated proprioceptive sensory axons and are thought to be inhibitory. However, we report here that activating GAD2+ neurons, directly with optogenetics or indirectly by cutaneous stimulation, facilitates sensory feedback to motoneurons in awake rodents and humans. GABAA receptors and GAD2+ contacts adjacent to nodes of Ranvier at branch points of sensory axons cause this facilitation, preventing spike propagation failure that is otherwise common without GABA. GABAA receptors are generally lacking from axon terminals (unlike GABAB) and do not inhibit transmitter release onto motoneurons, disproving the long-standing assumption that GABAA receptors cause presynaptic inhibition. GABAergic innervation of nodes near branch points allows individual branches to function autonomously, with GAD2+ neurons regulating which branches conduct, adding a computational layer to the neuronal networks generating movement and likely generalizing to other CNS axons.
Publisher
Cold Spring Harbor Laboratory
Cited by
8 articles.
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