TY - JOUR
T1 - A glutamate mechanism in the intermediolateral nucleus mediates sympathoexcitatory responses to stimulation of the rostral ventrolateral medulla
AU - Morrison, Shaun F.
AU - Ernsberger, Paul
AU - Milner, Teresa A.
AU - Callaway, Janie
AU - Gong, Anson
AU - Reis, Donald J.
N1 - Funding Information:
The authors wish to thank Drs. P. Petrusz and A. Rustioni (Department of Anatomy and Physiology, University of North Carolina at Chapel Hill) for the use of their glutamate antibody and J. Orefice for production of the illustrations. This research was supported by National Institutes of Health Grants HL 18974 and NS 22721.
PY - 1989/1/1
Y1 - 1989/1/1
N2 - The rostral ventrolateral medulla (RVL) contains a population of reticulospinal, sympathoexcitatory neurons. The regulation of the discharge of RVL-spinal vasomotor neurons by afferent pathways to the RVL underlies many reflex adjustments of circulation in response to peripheral and central stimuli. While vasomotor neurons of the RVL are presumed to exert their sympathoexcitatory effects over pathways terminating in the intermediolateral nucleus (IML) of the thoracolumbar spinal cord, little is known of the role played by specific spinal transmitter systems in mediating the increases in sympathetic nerve activity evoked by RVL neuronal discharge. This chapter discusses the combination of electrophysiological, immunocytochemical, and receptor autoradiographic techniques to test the hypothesis that an excitatory amino acid is the fast transmitter implicated in RVL-evoked excitation of sympathetic preganglionic neurons (SPNs). Results suggest that RVL stimulation causes the release of glutamate from nerve terminals in the IML that interacts with glutamate receptors of the kainate subtype to excite SPNs, thereby, producing an increase in sympathetic nerve activity and arterial pressure.
AB - The rostral ventrolateral medulla (RVL) contains a population of reticulospinal, sympathoexcitatory neurons. The regulation of the discharge of RVL-spinal vasomotor neurons by afferent pathways to the RVL underlies many reflex adjustments of circulation in response to peripheral and central stimuli. While vasomotor neurons of the RVL are presumed to exert their sympathoexcitatory effects over pathways terminating in the intermediolateral nucleus (IML) of the thoracolumbar spinal cord, little is known of the role played by specific spinal transmitter systems in mediating the increases in sympathetic nerve activity evoked by RVL neuronal discharge. This chapter discusses the combination of electrophysiological, immunocytochemical, and receptor autoradiographic techniques to test the hypothesis that an excitatory amino acid is the fast transmitter implicated in RVL-evoked excitation of sympathetic preganglionic neurons (SPNs). Results suggest that RVL stimulation causes the release of glutamate from nerve terminals in the IML that interacts with glutamate receptors of the kainate subtype to excite SPNs, thereby, producing an increase in sympathetic nerve activity and arterial pressure.
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U2 - 10.1016/S0079-6123(08)62006-3
DO - 10.1016/S0079-6123(08)62006-3
M3 - Article
C2 - 2575775
AN - SCOPUS:0024848182
SN - 0079-6123
VL - 81
SP - 159
EP - 169
JO - Progress in Brain Research
JF - Progress in Brain Research
IS - C
ER -