Abstract

The brain changes in response to sensory signals it is exposed to. It has been shown that long term potentiation-like neuroplasticity can be experimentally induced via visual paired-associative stimulation (V-PAS). V-PAS combines afferent visual stimuli with a transcranial magnetic stimulation pulse to induce plasticity. Preparation of a reaching movement to generate activity in superior parietal occipital cortex (SPOC) was used in this study as an additional afferent contributor to modulate the resultant plasticity. We hypothesized that V-PAS with a reaching movement would induce greater cortical excitability than V-PAS alone and would exhibit facilitated SPOC to M1 projections. All four experiments enrolled groups of 10 participants to complete variations of V-PAS in a repeated measures design. SPOC to M1 projections facilitated motor cortex excitability following V-PAS regardless of intervention received. We did not observe evidence indicating extra afferent information provided an additive effect to participants. Investigation of PMd to M1 projections confirmed disinhibition and suggested interneuronal populations within M1 may be mechanistically involved. Future research should look to rule out the existence of an upper limit for effective afference during V-PAS and investigate the average influence of V-PAS on cortical excitability in the larger population.

Highlights

  • superior parietal occipital cortex (SPOC)-M1 paired-pulse transcranial magnetic stimulation (TMS) was examined over eight different conditions generated by combinations of: time (Pre/Post intervention), activity (Active/rest and active state data (Rest)), and visual pairedassociative stimulation (V-Paired-associative stimulation (PAS))

  • The first is that SPOC to M1 projections tested at rest appear to be influenced by both resting and active V-PAS

  • Given that the effect size of either V-PAS intervention on resting Paired-pulse TMS (ppTMS) is nearly identical, it is likely there is a common effect present in both these measures which is independent of the type of V-PAS and depends rather only on the mechanisms of VPAS itself as a causal factor

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Summary

Introduction

A hallmark of the human brain is the ability to continuously adapt and learn from the environment through neuroplasticity It is becoming clear long-term potentiation (LTP) is critically involved in this process. PAS functions with the principle of Hebbian plasticity which formalizes the observation when one neuron repeatedly stimulates another neuron, the synapse between those neurons will change to strengthen that connection [1]. This mechanism is manufactured in PAS which pairs a sensory stimulus with a single pulse of transcranial magnetic stimulation (TMS) repeated over many trials. A common application of PAS stimulates the median nerve followed by a single TMS pulse 25 ms later [3,4,5,6]

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