CARDIAC SENSORY INTEGRATION IN CERVICAL SPINAL CORD
The long term objective of the proposed research is to provide an understanding of the central neural integration that could explain production or suppression of pain associated with myocardial ischemia. The focus of the current set of experiments is to analyze a specific group of cells in the first cervical to third cervical spinal segments that could inhibit transmission in the spinothalamic tract. The hypothesis is that high cervical neurons with descending projections are involved in processing sensory visceral information that inhibits nociceptive inputs and distant spinal segments.
Specific aims are designed to answer the following questions. 1) Does chemical stimulation or inactivation of neurons in high cervical segments affect activity of thoracic and lumbosacral spinothalamic tract neurons? 2) Are cervical propriospinal neurons excited by sensory visceral inputs that enter different spinal segments? 3) Does vagal stimulation excite cervical propriospinal neurons? 4) Are synaptic connections in medullary nucleus tractus solitarius needed for vagal effects in cervical neurons? 5) Are cervical propriospinal neurons excited by cardiac sensory information traveling in vagal fibers, sympathetic fibers or both types of afferent neural fibers? 6) Does myocardial ischemia affect activity of cervical propriospinal neurons?
Neurophysiological techniques will be used to address these aims. In the first specific aim, extracellular potentials of thoracic and lumbosacral spinothalamic tract neurons will be recorded in monkeys to determine effects of stimulating or inactivating cervical neurons. In Specific Aims 2-6, extracellular potentials of cervical propriospinal neurons with projections to thoracic or lumbar segments will be recorded in monkeys to determine responses to visceral stimuli.
The data derived from these studies will serve as a important basis for understanding the phenomenon of "silent" myocardial ischemia in humans. This project should provide insights into central neural mechanisms involved in suppression of visceral nociceptive information. Thus, these results are expected to provide a neurophysiological basis to explain the elevated pain threshold that is observed in patients who experience myocardial ischemia without pain and are at risk for sudden death.