Alternatively, studies in auditory cortex and hippocampus reveal an inverted-U relationship between VNS intensity and plasticity, where low and high intensity VNS drive little to no plasticity, while moderate intensity VNS significantly enhances plasticity. Thus, VNS intensity and plasticity may be linearly related, where higher intensities of VNS yield greater plasticity.

Increasing VNS intensity drives monotonic increases in neural activity in the locus coeruleus (LC), an area necessary for the effects of VNS on central nervous system.

For example, repeatedly pairing VNS with forelimb training increases forelimb representation in the motor cortex.Ī number of stimulation parameters influence the magnitude of plasticity driven by VNS in the auditory cortex, but the effect of these parameters on motor cortex plasticity remains largely unexplored. Repeatedly pairing VNS with a sensory or motor event drives robust, targeted cortical plasticity. VNS drives rapid engagement of the neuromodulators acetylcholine and norepinephrine, which act synergistically to strengthen synaptic connections in activated circuits. Thus, increasing the amount of VNS-mediated plasticity could lead to enhanced recovery. VNS is believed to promote recovery by inducing plasticity in networks activated during rehabilitation. Recovery is thought to be associated with plasticity in central networks after injury. Vagus nerve stimulation (VNS) has recently emerged as a method of enhancing rehabilitation for a wide range of neurological disorders affecting motor function including stroke, traumatic brain injury, and spinal cord injury.

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