Title:
Reorganization of Motor Cortex by Vagus Nerve Stimulation Requires Cholinergic Innervation.
Author:
Hulsey DR; Hays SA; Khodaparast N; Ruiz A; Das P; Rennaker RL 2nd; Kilgard MP.
Brain Stimulation. 9(2):174-81, 2016 Mar-Apr.
[Journal Article. Research Support, N.I.H., Extramural. Research Support, Non-U.S. Gov’t. Research Support, U.S. Gov’t, Non-P.H.S.] UI: 26822960
Background:
Vagus nerve stimulation (VNS) paired with forelimb training drives robust, specific reorganization of movement representations in the motor cortex. The mechanisms that underlie VNS-dependent enhancement of map plasticity are largely unknown. The cholinergic nucleus basalis (NB) is a critical substrate in cortical plasticity, and several studies suggest that VNS activates cholinergic circuitry.
Objective:
We examined whether the NB is required for VNS-dependent enhancement of map plasticity in the motor cortex. METHODS: Rats were trained to perform a lever pressing task and then received injections of the immunotoxin 192-IgG-saporin to selectively lesion cholinergic neurons of the NB. After lesion, rats underwent five days of motor training during which VNS was paired with successful trials. At the conclusion of behavioral training, intracortical microstimulation was used to document movement representations in motor cortex.
Results:
VNS paired with forelimb training resulted in a substantial increase in the representation of proximal forelimb in rats with an intact NB compared to untrained controls. NB lesions prevent this VNS-dependent increase in proximal forelimb area and result in representations similar to untrained controls. Motor performance was similar between groups, suggesting that differences in forelimb function cannot account for the difference in proximal forelimb representation.
Conclusions:
Together, these findings indicate that the NB is required for VNS-dependent enhancement of plasticity in the motor cortex and may provide insight into the mechanisms that underlie the benefits of VNS therapy.
Copyright © 2016 Elsevier Inc. All rights reserved.
Institutions:
Hulsey, Daniel R. School of Behavioral Brain Sciences, The University of Texas at Dallas, 800 West Campbell Road, GR41, Richardson, TX 75080- 3021, USA. Hays, Seth A.
School of Behavioral Brain Sciences, The University of Texas at Dallas, 800 West Campbell Road, GR41, Richardson, TX 75080-3021, USA; Erik Jonsson
School of Engineering and Computer Science, The University of Texas at Dallas, 800 West Campbell Road, Richardson, TX 75080-3021, USA; Texas
Biomedical Device Center, The University of Texas at Dallas, 800 West Campbell Road, Richardson, TX 75080-3021, USA. Electronic address: seth.hays@utdallas.edu.
Khodaparast, Navid. School of Behavioral Brain Sciences, The University of Texas at Dallas, 800 West Campbell Road, GR41, Richardson, TX 75080-3021, USA;Texas Biomedical Device Center, The University of Texas at Dallas, 800 West Campbell Road, Richardson, TX 75080-3021, USA. Ruiz, Andrea.
Texas Biomedical Device Center, The University of Texas at Dallas, 800 West Campbell Road, Richardson, TX 75080-3021, USA. Das, Priyanka. Erik
Jonsson School of Engineering and Computer Science, The University of Texas at Dallas, 800 West Campbell Road, Richardson, TX 75080-3021, USA.
Rennaker, Robert L 2nd. School of Behavioral Brain Sciences, The University of Texas at Dallas, 800 West Campbell Road, GR41, Richardson, TX 75080-3021, USA; Erik Jonsson School of Engineering and Computer Science, The University of Texas at Dallas, 800 West Campbell Road, Richardson, TX 75080-3021, USA; Texas Biomedical Device Center, The University of Texas at Dallas, 800 West Campbell Road, Richardson, TX 75080-3021, USA.
Kilgard, Michael P. School of Behavioral Brain Sciences, The University of Texas at Dallas, 800 West Campbell Road, GR41, Richardson, TX 75080- 3021, USA; Texas Biomedical Device Center, The University of Texas at Dallas, 800 West Campbell Road, Richardson, TX 75080-3021, USA.
