C-fos expression and electrolytic lesions studies reveal activation of the posterior region of Locus Coeruleus during hemorrhage induced hypotension

Locus Coeruleus Lesions Decrease Oxytocin and Vasopressin Release Induced by Hemorrhage

“…Data showing that LC lesion did not affect basal secretion of AVP and OT are in accordance with previous studies reporting that LC does not participate in the control of several physiological parameters such as basal blood pressure or the basal secretion of various hormones during resting states, but it is important in situations of physiological challenges [16,25,26]. In fact, LC is activated by several stressful stimuli, such as hemorrhage, pain and immobilization, which are known to induce increases in Fos protein expression and tyrosine hydroxylase mRNA in that nucleus [27,28].…”

“…Some studies assign them a pressor role [8][9][10] whereas others give them a depressor role [11][12][13] or even suggest no role for that nucleus in such regulation [14,15]. Previous research in our laboratory demonstrated that LC lesions accentuated the hypotensive response to hemorrhage [16]. In this study, we investigated the participation of LC on the hemorrhageinduced AVP and OT secretion in rats.…”

Locus coeruleus noradrenergic neurons and CO2 drive to breathing

“…Stimulation of the LC by local microinjection of L-glutamate [61], L-arginine, a precursor of nitric oxide [69], or adenosine triphosphate [70] causes hypotension and bradycardia. Other reports demonstrate that there are no cardiovascular changes after inhibition of the LC neurons by local microinjection of N-methyl-D-aspartate receptor antagonist, nitric oxide synthase inhibitors [69], neuroinhibitory agents such as gamma-aminobutyric acid or muscimol [39,61], α 2 -adrenoceptor antagonist [70], or by bilateral electrolytic lesions of this nucleus [3]. Our study demonstrated that chemical lesion of the LC with 6-OHDA did not affect basal arterial pressure and HR, indicating that noradrenergic LC neurons are unlikely to play a significant role in the maintenance of resting blood pressure and HR.…”

“…It is estimated that~50% of all the noradrenergic projections in the central nervous system originate in the LC [8,13]. Consequently, LC is implicated not only in the control of breathing [16,20,29,32,47,64] but also in the control of many homeostatic functions including thermoregulation [2,21,53] and cardiovascular function [3,40,41,61,65].…”

“…Regarding cardiovascular function, there is evidence that hypercapnia increases mean arterial blood pressure in dogs [55] and rats [28], and LC may be a structure in the central nervous system involved in the mediation of this response [3,40,41,61,65].…”