Enhancing plasticity in central networks improves motor and sensory recovery after nerve damage.

Author: Meyers EC1, Kasliwal N2, Solorzano BR2, Lai E3, Bendale G4, Berry A2, Ganzer PD2, Romero-Ortega M2,3,4, Rennaker RL 2nd2,3,4, Kilgard MP2,3,4, Hays SA2,3,4
Affiliation:
1Texas Biomedical Device Center, The University of Texas at Dallas, 800 West Campbell Road, Richardson, TX, 75080-3021, USA. eric.meyers@utdallas.edu.
2Texas Biomedical Device Center, The University of Texas at Dallas, 800 West Campbell Road, Richardson, TX, 75080-3021, USA.
3School of Behavioral and Brain Sciences, The University of Texas at Dallas, 800 West Campbell Road, Richardson, TX, 75080-3021, USA.
4Department of Bioengineering, Erik Jonsson School of Engineering and Computer Science, The University of Texas at Dallas, 800 West Campbell Road, Richardson, TX, 75080-3021, USA.
Conference/Journal: Nat Commun.
Date published: 2019 Dec 19
Other: Volume ID: 10 , Issue ID: 1 , Pages: 5782 , Special Notes: doi: 10.1038/s41467-019-13695-0. , Word Count: 149


Nerve damage can cause chronic, debilitating problems including loss of motor control and paresthesia, and generates maladaptive neuroplasticity as central networks attempt to compensate for the loss of peripheral connectivity. However, it remains unclear if this is a critical feature responsible for the expression of symptoms. Here, we use brief bursts of closed-loop vagus nerve stimulation (CL-VNS) delivered during rehabilitation to reverse the aberrant central plasticity resulting from forelimb nerve transection. CL-VNS therapy drives extensive synaptic reorganization in central networks paralleled by improved sensorimotor recovery without any observable changes in the nerve or muscle. Depleting cortical acetylcholine blocks the plasticity-enhancing effects of CL-VNS and consequently eliminates recovery, indicating a critical role for brain circuits in recovery. These findings demonstrate that manipulations to enhance central plasticity can improve sensorimotor recovery and define CL-VNS as a readily translatable therapy to restore function after nerve damage.

PMID: 31857587 DOI: 10.1038/s41467-019-13695-0

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