Date of Award
1996
Degree Type
Dissertation
Degree Name
Doctor of Philosophy
Abstract
Three series of experiments were done to investigate the output pathways from the central nucleus of the amygdala (ACe) involved in the control of arterial pressure. The first series of experiments provided the first demonstration that the arterial pressure responses elicited during stimulation of ACe were mediated via a direct pathway to the bed nucleus of the stria terminalis (BST). Microinjection of retrograde tract tracers into depressor regions of BST resulted in labelled neurons within predominantly the lateral subdivision of ACe. In addition, iontophoresis of the anterograde tract tracer PHA-L into cardiovascular responsive regions of ACe resulted in fiber and presumptive terminal labelling within the cardiovascular responsive region of BST. Furthermore, the depressor responses elicited during stimulation of ACe were attenuated after blocking synaptic transmission BST.;The second series of experiments showed unequivocally that ACe neurons received inputs from the ventrolateral medulla (VLM). Using retrograde and anterograde tract tracers in combination with immunohistochemistry for the catecholamine biosynthetic enzymes, it was demonstrated that the A1 noradrenergic cell group in VLM predominantly innervated ACe. In addition, stimulation of sites within VLM that overlapped this catecholaminergic cell group were shown to alter the discharge rate of 47% of spontaneously active single units in ACe. Of these units 44% also responded to baroreceptor afferent inputs.;The third series of experiments provided evidence for inputs to ACe neurons that may function to modulate the cardiovascular output from ACe. Single units in ACe that were silent and were antidromically activated by stimulation of cardiovascular responsive sites within BST did not respond orthodromically to VLM and baroreceptor afferent inputs. However, it was demonstrated that ACe units (6/12) that projected directly to BST responded orthodromically to stimulation of insular cortex or paraventricular nucleus of the thalamus. Microinjections of L-glutamate into ACe in the presence of tyramine or noradrenaline within ACe, significantly attenuated the depressor responses elicited from ACe. In addition, GABAergic neurons in ACe were also shown for the first time to alter the cardiovascular output from ACe.;These data have provided evidence for a cardiovascular pathway from ACe to BST that may be modulated by noradrenergic inputs from VLM.
Recommended Citation
Roder, Stefanie, "Limbic Mechanisms Controlling Arterial Pressure" (1996). Digitized Theses. 2625.
https://ir.lib.uwo.ca/digitizedtheses/2625