Lateral parabrachial afferent areas and serotonin mechanisms activated by volume expansion.
Recent evidence has shown that the serotonergic mechanism of the lateral parabrachial nucleus (LPBN) participates in the regulation of renal and hormonal responses to isotonic blood volume expansion (BVE). We investigated the BVE-induced Fos activation along forebrain and hindbrain nuclei and particularly within the serotonergic clusters of the raphé system that directly project to the LPBN. We also examined whether there are changes in the concentration of serotonin (5HT) within the raphé nucleus in response to the same stimulus. With this purpose, we analyzed the cells doubly labeled for Fos and Fluorogold (FG) following BVE (NaCl 0.15 M, 2 ml/100 g b.w., 1 min) 7 days after FG injection into the LPBN. Compared with the control group, blood volume-expanded rats showed a significant greater number of Fos-FG double-labeled cells along the nucleus of the solitary tract, locus coeruleus, hypothalamic paraventricular nucleus, central extended amygdala complex, and dorsal raphé nucleus (DRN) cells. Our study also showed an increase in the number of serotonergic DRN neurons activated in response to isotonic BVE. We also observed decreased levels of 5HT and its metabolite 5-hydroxyindoleacetic acid (measured by high-pressure liquid chromatography) within the raphé nucleus 15 min after BVE. Given our previous evidence on the role of the serotonergic system in the LPBN after BVE, the present morphofunctional findings suggest the existence of a key pathway (DRN-LPBN) that may control BVE response through the modulation of 5HT release.
Margatho
Lisandra Oliveira
LO
Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo (USP), São Paulo, Brazil.
Godino
Andrea
A
Oliveira
Fabíola Raquel Tenório
FR
Vivas
Laura
L
Antunes-Rodrigues
José
J
D000818:Animals; D017776:Autonomic Pathways / Q000166:cytology / Q000378:metabolism*; D015415:Biomarkers / Q000032:analysis / Q000378:metabolism; D001794:Blood Pressure / Q000502:physiology; D001810:Blood Volume / Q000187:drug effects / Q000502:physiology*; D001931:Brain Mapping; D006897:Hydroxyindoleacetic Acid / Q000378:metabolism; D006973:Hypertension / Q000503:physiopathology; D008297:Male; D011149:Pons / Q000166:cytology / Q000378:metabolism*; D017729:Presynaptic Terminals / Q000378:metabolism; D016760:Proto-Oncogene Proteins c-fos / Q000032:analysis / Q000378:metabolism; D011903:Raphe Nuclei / Q000166:cytology / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D012701:Serotonin / Q000378:metabolism*; D012965:Sodium Chloride / Q000494:pharmacology; D013194:Staining and Labeling; D013266:Stilbamidines; D009435:Synaptic Transmission / Q000502:physiology; D015854:Up-Regulation / Q000187:drug effects / Q000502:physiology; D017833:Visceral Afferents / Q000166:cytology / Q000378:metabolism*; D014882:Water-Electrolyte Balance / Q000187:drug effects / Q000502:physiology
C049774:2-hydroxy-4,4'-diamidinostilbene, methanesulfonate salt; D015415:Biomarkers; D016760:Proto-Oncogene Proteins c-fos; D013266:Stilbamidines; D012701:Serotonin; D012965:Sodium Chloride; D006897:Hydroxyindoleacetic Acid