Dampney R A, Blessing W W, Tan E
Department of Physiology, University of Sydney, N.S.W., Australia.
J Auton Nerv Syst. 1988 Oct;24(3):227-39. doi: 10.1016/0165-1838(88)90123-3.
The aims of this study were to determine (1) whether the vasomotor effects reflexly elicited by baroreceptor stimulation are dependent upon gamma-aminobutyric acid (GABA) receptors in the subretrofacial (SRF) nucleus in the rostral ventrolateral medulla; (2) the extent to which inputs other than those arising from peripheral baroreceptors, or transmitted via the nucleus tractus solitarius (NTS), contribute to the tonic GABAergic inhibition of SRF vasopressor cells. Following bilateral injection of a mixture of the GABA antagonist bicuculline methiodide (500 pmol) and GABA agonist muscimol (500 pmol) into the SRF nucleus, the sympathoinhibitory response normally evoked by a rise in arterial pressure (induced by inflating an aortic cuff) was abolished in 4 out of 8 rabbits and reduced in the remainder. For the whole group, the mean reduction in this response was 71%. In other experiments, the pressor response produced by injection of bicuculline methiodide into the SRF nucleus was still present after (1) destruction of the intermediate portion of the NTS, and (2) complete removal of the brain rostral to the pons. We conclude that (1) an inhibitory GABAergic input into the SRF nucleus is an important component of the central pathways mediating baroreceptor inhibition of sympathetic vasomotor tone; (2) the SRF nucleus also receives tonic GABAergic inputs that are intrinsic to the lower brainstem and are independent of baroreceptor or other cardiovascular inputs relayed by the NTS.
