Circuits for Grasping: Spinal dI3 Interneurons Mediate Cutaneous Control of Motor Behavior

Accurate motor performance depends on the integration in spinal microcircuits of sensory feedback information. Hand grasp is a skilled motor behavior known to require cutaneous sensory feedback, but spinal microcircuits that process and relay this feedback to the motor system have not been defined....

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Veröffentlicht in:Neuron (Cambridge, Mass.) Mass.), 2013-04, Vol.78 (1), p.191-204
Hauptverfasser: Bui, Tuan V., Akay, Turgay, Loubani, Osama, Hnasko, Thomas S., Jessell, Thomas M., Brownstone, Robert M.
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Sprache:eng
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Zusammenfassung:Accurate motor performance depends on the integration in spinal microcircuits of sensory feedback information. Hand grasp is a skilled motor behavior known to require cutaneous sensory feedback, but spinal microcircuits that process and relay this feedback to the motor system have not been defined. We sought to define classes of spinal interneurons involved in the cutaneous control of hand grasp in mice and to show that dI3 interneurons, a class of dorsal spinal interneurons marked by the expression of Isl1, convey input from low threshold cutaneous afferents to motoneurons. Mice in which the output of dI3 interneurons has been inactivated exhibit deficits in motor tasks that rely on cutaneous afferent input. Most strikingly, the ability to maintain grip strength in response to increasing load is lost following genetic silencing of dI3 interneuron output. Thus, spinal microcircuits that integrate cutaneous feedback crucial for paw grip rely on the intermediary role of dI3 interneurons. ► Spinal dI3 interneurons are glutamatergic and project to motoneurons ► dI3 interneurons receive direct primary afferent inputs from cutaneous afferents ► Silencing the output of dI3 interneurons disrupts a disynaptic cutaneous reflex ► dI3 interneurons mediate cutaneous control of paw grasp Bui et al. identify a microcircuit in the mouse spinal cord involved in cutaneous regulation of motor control. Using genetic strategies, they demonstrate that removing dI3 interneuron function from this circuit impairs the ability of mice to regulate grip strength.
ISSN:0896-6273
1097-4199
DOI:10.1016/j.neuron.2013.02.007