Received September 14, 2005
Revised September 20, 2005
Accepted after revision October 5, 2005

¹ University of Missouri

^* To whom correspondence should be addressed. E-mail: pottsjt{at}missouri.edu.

	Abstract

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 by 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 -aminobutyric acid (GABA) inhibitory neurotransmission within the NTS plays 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 neurons; and 2) excitation of sympathoexcitatory neurons in the rostral ventrolateral medulla. Current research findings will be discussed that support an interaction between GABA and substance P (SP) signaling 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.

Key Words: Arterial baroreflex, Muscle contraction, Nucleus tractus solitarii

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