Key result
Serial NTS-CVL-RVL neural pathway critically inhibits sympathetic outflow after baroreceptor stimulation in rats.
This review outlines the fundamental neuronal substrates and pathways involved in the arterial baroreceptor reflex in rats.
Should not inform clinical baroreflex interventions; leaves open human translation while extending rodent NTS-CVL-RVL pathway mapping.
The fundamental neuronal substrates of the arterial baroreceptor reflex have been elucidated by combining anatomical, neurophysiological, and pharmacological approaches. A serial pathway between neurons located in the nuclei of the solitary tract (NTS), the caudal ventrolateral medulla (CVL), and the rostral ventrolateral medulla (RVL) plays a critical role in inhibition of sympathetic outflow following stimulation of baroreceptor afferents. In this paper, we summarize our studies using tract-tracing and electron microscopic immunocytochemistry to define the potential functional sites for synaptic transmission within this circuitry. The results are discussed as they relate to the literature showing: (1) baroreceptor afferents excite second-order neurons in NTS through the release of glutamate; (2) these NTS neurons in turn send excitatory projections to neurons in the CVL; (3) GABAergic CVL neurons directly inhibit RVL sympathoexcitatory neurons; and (4) activation of this NTS-->CVL-->RVL pathway leads to disfacilitation of sympathetic preganglionic neurons by promoting withdrawal of their tonic excitatory drive, which largely arises from neurons in the RVL. Baroreceptor control may also be regulated over direct reticulospinal pathways exemplified by a newly recognized sympathoinhibitory region of the medulla, the gigantocellular depressor area. This important autonomic reflex may also be influenced by parallel, multiple, and redundant networks.
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Aicher et al. (2000) conducted a review in Arterial baroreceptor reflex. A serial pathway between neurons in the NTS, CVL, and RVL plays a critical role in the inhibition of sympathetic outflow following stimulation of baroreceptor afferents in the rat.
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