Inhibitory neurotransmission in the nucleus tractus solitarii: implications for baroreflex resetting during exercise

• Published in: Experimental physiology 2006-01, Vol.91 (1), p.59-72
• Main Author: Potts, Jeffrey T.
• Format: Article
• Language: English
• Subjects: Afferent Pathways - metabolism; Animals; Baroreflex - physiology; Blood Pressure; Cardiovascular System - innervation; Exercise - physiology; gamma-Aminobutyric Acid - metabolism; Glutamic Acid - metabolism; Heart Rate; Humans; Interneurons - metabolism; Muscle, Skeletal - innervation; Neural Inhibition; Posterior Horn Cells - metabolism; Pressoreceptors - physiology; Receptors, Glutamate - metabolism; Receptors, Neurokinin-1 - metabolism; Solitary Nucleus - metabolism; Solitary Nucleus - physiology; Substance P - metabolism
• ISSN: 0958-0670; 1469-445X
• DOI: 10.1113/expphysiol.2005.032227

Inhibitory neurotransmission plays a crucial role in the processing of sensory afferent signals in the nucleus of the solitary tract (NTS). The aim of this review is to provide a critical overview of inhibitory mechanisms that may be responsible for altering arterial baroreflex function during physical activity or exercise. Over a decade ago, the view of reflex control of cardiovascular function during exercise was revised because of the finding that the arterial baroreflex is reset in humans, enabling continuous beat-to-beat reflex regulation of blood pressure and heart rate. During the ensuing decade, many investigators proposed that resetting was mediated by central neural mechanisms that were intrinsic to the brain. Recent experimental data suggest that rapid and reversible changes in γ-aminobutyric acid (GABA) inhibitory neurotransmission within the NTS play a fundamental role in this process. The hypothesis will be presented that baroreflex resetting by somatosensory input is mediated by: (1) selective inhibition of barosensitive NTS neurones; and (2) excitation of sympathoexcitatory neurones in the rostral ventrolateral medulla. Current research findings will be discussed that support an interaction between GABA and substance P (SP) signalling mechanisms in the NTS. An understanding of these mechanisms may prove to be essential for future detailed analysis of the cellular and molecular mechanisms underlying sensory integration in the NTS.