We review our approach to functionally identifying cortical and subcortical areas involved in the generation of spontaneous fluctuations in sympathetic outflow to muscle or skin. We record muscle sympathetic nerve activity (MSNA) or skin sympathetic nerve activity (SSNA), via a tungsten microelectrode inserted percutaneously into the common peroneal nerve, at the same time as performing functional magnetic resonance imaging (fMRI) of the brain. By taking advantage of the neurovascular coupling delay associated with BOLD (Blood Oxygen Level Dependent) fMRI, and the delay associated with conduction of a burst of sympathetic impulses to the peripheral recording site, we can identify structures in which BOLD signal intensity covaries with MSNA or SSNA. Using this approach we have shown that signal intensity and MSNA were positively correlated in the left mid-insula, bilateral dorsolateral prefrontal cortex, bilateral posterior cingulate cortex, bilateral precuneus, left dorsomedial hypothalamus, bilateral ventromedial hypothalamus and bilateral rostral ventrolateral medualla. Conversely, spontaneous bursts of SSNA covaried with BOLD signal intensity in the left ventromedial thalamus, the left posterior and right anterior insula, the right orbitofrontal cortex, right frontal cortex, and bilaterally in the mid-cingulate cortex and precuneus. These results emphasize the contributions of cortical regions of the brain to sympathetic outflow in awake human subjects, and the extensive interactions between cortical and subcortical regions in the ongoing regulation of sympathetic nerve activity to muscle and skin in awake human subjects.
- sympathetic nerve activity
- Copyright © 2015, Journal of Neurophysiology