A New Signal Processing Approach to Study Action Potential Content in Sympathetic Neural Signals

Sympathetic nerve activity plays an essential role in the normal regulation of blood pressure in humans and in the etiology and progression of many chronic diseases. Sympathetic nerve recordings associated with blood pressure regulation can be recorded directly using microneurography. A general characteristic of this signal is spontaneous burst activity of spikes (action potentials) separated by silent periods against a background of considerable gaussian noise. During measurement with electrodes, the raw muscle sympathetic nerve activity (MSNA) signal is amplified, band-pass filtered, rectified and integrated. This integration process removes important information regarding action potential content and their discharge properties. The first objective of this thesis was to propose a new method for detecting action potentials from the raw MSNA signal to enable investigation of post-ganglionic neural discharge properties. The new method is based on the design of a mother wavelet that is matched to an actual mean action potential template extracted from a raw MSNA signal and applying it to the raw MSNA signal using a continues wavelet transform (CWT) for spike detection. The performance of the proposed method versus two previous wavelet-based approaches was evaluated using 1) MSNA recorded from seven healthy participants and, 2)simulated MSNA. The results show that the new matched wavelet performs better than the previous wavelet-based methods that use a non-matched wavelet in detecting action potentials in the MSNA signal. The second objective of this thesis was to employ the proposed action potential detection and classification technique to study the relationship between the recruitment of sympathetic action potentials (i.e., neurons) and the size of integrated sympathetic bursts in human MSNA signal. While in other neural systems (e.g. the skeletal motor system) there is a well understood pattern of neural recruitment during activation, our understanding of how sympathetic neurons are coordinated during baseline and baroreceptor unloading are very limited. We demonstrate that there exists a hierarchical pattern of recruitment of additional faster conducting neurons of larger amplitude as the sympathetic bursts become stronger. This information has important implications for how blood pressure is controlled, and the malleability of sympathetic activa-

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