title: Contribution of bed nucleus of the stria terminalis to the cardiovascular responses elicited by stimulation of the amygdala.
abstract: Anatomical and physiological studies were done in the rat to investigate the possibility that the cardiovascular responses elicited by stimulation of central nucleus of the amygdala (ACe) were mediated via projections to bed nucleus of the stria terminalis (BST). In the first series, to determine the distribution of neurons in ACe that projected to the cardiovascular region of BST, the retrograde tracer Fluorogold (FG) or rhodamine latex micro-beads (Rd) were injected into BST. FG and Rd injections that overlapped the cardiovascular region of BST resulted in retrogradely labelled neurons throughout the amygdala. In ACe, retrogradely labelled neurons were observed primarily in the lateral subdivision of the rostral ACe compared to the caudal ACe. The medial subdivision of ACe was found to have very few retrogradely labelled neurons. In the second series, the effect of either blocking synaptic transmission in BST with CoCl2, chemical lesions of BST with ibotenic acid (IBO), or electrolytic lesions of BST on the depressor response elicited by either electrical or chemical stimulation of ACe was investigated in the chloralose-anesthetized, artificially ventilated and paralysed rat. Microinjections of CoCl2 into BST significantly attenuated the depressor responses to stimulation of the rostral components of the lateral subnucleus of ACe, but not those to stimulation of the caudal and medial components of ACe. Microinjections of IBO into BST or electrolytic lesions of BST resulted in similar effects on the depressor responses to ACe stimulation. Taken together, these data indicate that neurons within the rostral components of the lateral subnucleus of ACe project to the cardiovascular region of BST and mediate in part the depressor responses to stimulation of the rostral ACe. On the other hand, the depressor responses elicited from the caudal ACe are not mediated through BST. These results suggest that at least two independent pathways originate in the ACe that influence the circulation.
authors.affiliation: Department of Physiology Health Science Centre University of Western Ontario, London, Canada.
authors.forename: S
authors.initials: S
authors.lastname: Roder
authors.forename: J
authors.initials: J
authors.lastname: Ciriello
mesh_terms: D000679:Amygdala / Q000502:physiology*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D003035:Cobalt / Q000494:pharmacology; D004558:Electric Stimulation; D004566:Electrodes; D005456:Fluorescent Dyes; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000502:physiology*; D006651:Histocytochemistry; D007051:Ibotenic Acid / Q000494:pharmacology; D008297:Male; D008863:Microspheres; D051381:Rats; D017208:Rats, Wistar; D012235:Rhodamines; D013266:Stilbamidines; D013268:Stimulation, Chemical; D013569:Synapses / Q000187:drug effects; D013787:Thalamic Nuclei / Q000033:anatomy & histology / Q000502:physiology*
chemical_list: C049774:2-hydroxy-4,4'-diamidinostilbene, methanesulfonate salt; D005456:Fluorescent Dyes; D012235:Rhodamines; D013266:Stilbamidines; D007051:Ibotenic Acid; D003035:Cobalt; C018021:cobaltous chloride