INVESTIGATING THE FUNCTIONAL RELEVANCE OF AFFERENT INHIBITION

Abstract

Afferent inhibition is a phenomenon observed when an afferent volley evoked by peripheral nerve stimulation inhibits descending corticospinal output. Notably, this phenomenon is not observed in special populations exhibiting impairments in cognitive and/or sensorimotor function, suggesting that it plays an important role in normal human function. The overall goal of this thesis was to contribute new knowledge to the understanding of afferent inhibition. This was achieved by investigating the functional relevance of afferent inhibition and exploring methods for improving data acquisition. In study 1, I examined the relationship between long-latency afferent inhibition (LAI) and sensory afference, and determined the optimal stimulation parameters that would evoke maximal LAI. In study 2, I sought to determine the underlying neurotransmitter basis of afferent inhibition. The results showed that both LAI and short-latency afferent inhibition (SAI) are modulated by GABAA receptor activity but not GABAB receptor activity. Study 3 showed that these measures of afferent inhibition have poor-to-moderate reliability with moderately high levels of within-subject variability. In study 4, I investigated the relationship between afferent inhibition and glucose function. I found that ingestion of a glucose bolus does not modulate the magnitude or variability of afferent inhibition. In study 5, I explored the role of afferent inhibition in motor cortex organization. The results suggest that afferent inhibition may not be a mediator of motor cortex reorganization that occurs following sensory enrichment. Finally, I proposed a model of the neural pathways underlying SAI and LAI that would lead to inhibition of corticospinal output. The findings from this thesis contribute new knowledge to the afferent inhibition literature that will be useful for improving future study methodologies and understanding the linkage to human function.