Brain Pathways Involved in the Modulatory Effects of Noradrenaline in Lateral Septal Area on Cardiovascular Responses

Abstract

We have previously reported that stimulation of alpha-1 adrenoceptors by noradrenaline (NA) injected into the lateral septal area (LSA) of anaesthetized rats causes pressor and bradycardic responses that are mediated by acute vasopressin release into the circulation through activation of the paraventricular nucleus (PVN). Although the PVN is the final structure of this pathway, the LSA has no direct connections with the PVN, suggesting that other structures may connect these areas. To address this issue, the present study employed c-Fos immunohistochemistry to investigate changes caused by NA microinjection into the LSA in neuronal activation in brain structures related to systemic vasopressin release. NA microinjected in the LSA caused pressor and bradycardic responses, which were blocked by intraseptal administration of a-1 adrenoceptor antagonist (WB4101, 10 nmol/200 nL) or systemic V-1 receptor antagonist (dTyr(CH2)5(Me)AVP, 50 lg/kg). NA also increased c-Fos immunoreactivity in the prelimbic cortex (PL), infralimbic cortex (IL), dorsomedial periaqueductal gray (dmPAG), bed nucleus of the stria terminalis (BNST), PVN, and medial amygdala (MeA). No differences in the diagonal band of Broca, cingulate cortex, and dorsolateral periaqueductal gray (dlPAG) were found. Systemic administration of the vasopressin receptor antagonist dTyr AVP (CH2)5(Me) did not change the increase in c-Fos expression induced by intra-septal NA. This latter effect, however, was prevented by local injection of the alpha-1 adrenoceptor antagonist WB4101. These results suggest that areas such as the PL, IL, dmPAG, BNST, MeA, and PVN could be part of a circuit responsible for vasopressin release after activation of alpha-1 adrenoceptors in the LSA.

The medial amygdaloid nucleus is involved in the cardiovascular pathway activated by noradrenaline into the lateral septal area of rats

“…Despite all the evidence described above, our results show that the DBB is not part of the cardiovascular pathway activated by microinjection of NA into LSA. In agreement with our results, NA microinjected into the LSA increase c‐Fos expression in MeA but not in DBB (Scopinho et al. , 2012), suggesting that MeA is involved in the modulation of cardiovascular responses caused by LSA stimulation with NA, while DBB is probably not involved.…”

Reporter mouse strain provides a novel look at angiotensin type-2 receptor distribution in the central nervous system

“…A lateral septum to MeA pathway has been found to regulate cardiovascular homeostasis (Scopinho et al 2012). Furthermore, the lateral septum is a part of a pressor pathway that originates in the cingulate cortex (Fernandes et al 2005).…”

Mechanisms in the Bed Nucleus of the Stria Terminalis Involved in Control of Autonomic and Neuroendocrine Functions: A Review

“…Considering that the LSA does not project directly to PVN [204], and connections have been described between the BST and this hypothalamic structure [14], the BST could be a relay in the pathway of vasopressin release by the LSA. However, although noradrenaline microinjection into the LSA activate local BNST neurons [205], functional findings demonstrated that BNST inhibition did not affect cardiovascular responses to noradrenaline into the LSA [206]. Since other forebrain structures connected with BNST, such as MPFC and MeA, also modulates cardiovascular function through control of vasopressin release [197, 207], further studies are necessary to clarify the neural circuitry that the BNST is part.…”