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ALDOSTERONE INFUSION INTO THE 4 TH VENTRICLE PRODUCES ACTIVATION OF HSD2 NEURONS IN THE NTS AND SODIUM APPETITE
Author(s) -
Gasparini Silvia,
Melo Mariana Rosso,
AndradeFranze Glaucia Maria Fabricio,
Menani Jose Vanderlei,
Colombari Eduardo
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.1028.3
Subject(s) - aldosterone , median preoptic nucleus , lateral parabrachial nucleus , supraoptic nucleus , endocrinology , solitary tract , medicine , thirst , central nucleus of the amygdala , area postrema , chemistry , subfornical organ , sodium , hypothalamus , nucleus , sed , homeostasis , appetite , preoptic area , angiotensin ii , parabrachial nucleus , biology , central nervous system , blood pressure , neuroscience , organic chemistry
Aim Aldosterone sensitive neurons characterized by the presence of the enzyme HSD2 are present in the nucleus of the solitary tract (NTS) near to the 4 th V. These neurons are activated under various conditions that stimulate sodium intake, suggesting that they may have a role in sodium homeostasis. A recent study showed that chronic infusion of low dose of aldosterone into the 4 th ventricle (4 th V) induces sodium intake. Indeed, in the present study, we sought to investigate if the dose of aldosterone that induces sodium intake when infused into the 4 th V also activates HSD2 neurons in the NTS. In addition, it was also analyzed the activation of other areas of the brain important for the control fluid‐electrolyte balance and directly or indirectly connected with the NTS, like the lateral parabrachial nucleus (LPBN), central amygdala (CeA), supraoptic nucleus (SON), paraventricular nucleus (PVN) and medial preoptic nucleus (MPO). Material and Methods Male Holtzman rats with stainless steel cannulas implanted into the 4 th V were used. Rats had free access to water and food and also to 1.8% NaCl during 2 hours/day. Water and 1.8% NaCl intake was measured in the first 5 days of infusion of vehicle or aldosterone (100 ng/μl/h) into the 4 th V. On the sixth day of infusion, the brains were removed and the number of neurons expressing c‐Fos or c‐Fos and the enzyme HSD2 were quantified in different areas of the brain by immunohistochemistry. Results Chronic infusion of aldosterone (100 ng/h) into the 4 th V increased 1.8% NaCl intake (10.3 ± 3, vs. vehicle: 2.3 ± 1 ml/2 h), without changing water intake. The infusion of aldosterone into the 4 th V increased c‐Fos expression in HSD2 neurons in the intermediate NTS (3 ± 1, vs. vehicle: 0 ± 0 cells/section, p < 0.05) and rostral NTS (7 ± 2 vs. vehicle: 0 ± 0 cells/section, p < 0.05). The expression of c‐Fos also increased in non HSD2 neurons in the commissural NTS (22 ± 6, vs. vehicle: 5 ± 3 cells/section, p < 0.05). Aldosterone into the 4 th V also increased c‐Fos expression in the SON (21 ± 2, vs. vehicle 7 ± 2 cells/section, p < 0.05), CeA (29 ± 9, vs. vehicle: 0 ± 0 cells/section, p < 0.05), without changing c‐Fos expression in the LPBN (14 ± 4, vs. vehicle: 13 ± 5 cells/section, p > 0.05). PVN (23 ± 5, vs. vehicle: 10 ± 4 cells/section, p > 0.05) or MPO (22 ± 5, vs. vehicle 7 ± 7 cells/section, p > 0.05. Conclusion The activation of HSD2 neurons in the NTS by aldosterone infused into the 4 th V probably activates a central circuitry involved in the stimulation of sodium intake that may include one or more areas like SON and CeA. Support or Funding Information PROPE‐UNESP; CAPES; CNPq; FAPESP