Riley Zeller-Townson

Ph.D. Thesis  Defense

Date:  Thursday, August 16, 2018
Time: 1:00 PM
Location: Whitaker 3115 (McIntire Conference Room)

Thesis committee members:
Advisor: Dr. Robert Butera, PhD (Georgia Institute of Technology)
Dr. Garrett Stanley, PhD (Georgia Institute of Technology)
Dr. Chris Rozell, PhD (Georgia Institute of Technology)
Dr. Morten Raastad, MD, PhD (Emory University)
Dr. Bilal Haider, PhD (Georgia Institute of Technology)

Title: Measurement of activity-dependent response to electrical stimulation in small unmyelinated axons

Abstract:  While the dynamics of neural excitability are well understood for a short sequences of electrical stimuli, responses to repeated stimulation, such as used by clinical neural stimulators, can quickly become extremely difficult to predict.  The problem emerges as each responding action potential activates a set of activity-dependent mechanisms, which in turn may alter the excitability of the neuron and cause stimulation response to become intermittent.  The situation is further complicated by the fact that responses to electrical stimulation in small unmyelinated axons of cortex are often measured through indirect means, such as population activity. These measurements may confound stimulation reliability with other features of neural response, such as action potential waveform or conduction velocity, which are also modulated by activity-dependent processes.  Here, we show how high-density microelectrode arrays, a novel electrophysiology tool, can be used to tease apart these components of intermittent response to electrical stimulation.  We then use these tools to probe the impact of the stimulus location relative to the neuron on intermittent response, and investigate the role of the delay between stimulus and action potential initiation in measurements of response latency.  Based on our results, we argue that intermittent responsiveness to stimulation is a phenomena governed by spatially local dynamics, rather than cell-wide dynamics.  We then discuss implications of this claim for clinical neural stimulation, as well as the interpretation of antidromic latency measurements as evidence of timing plasticity.