title: Estrogen decreases the responsiveness of subfornical organ neurons to angiotensinergic neural inputs from the lateral hypothalamic area in the female rat.
abstract: Twenty-eight subfornical organ (SFO) neurons in ovariectomized (OVX) female rats that were treated with propylene glycol (PG) vehicle and 26 SFO neurons in OVX female rats that were treated with estrogen benzoate (EB) were antidromically activated by electrical stimulation of the hypothalamic paraventricular nucleus (PVN) under urethane anesthesia. No significant differences were observed between the PG-treated and EB-treated OVX animals in the latency, conduction velocity, or threshold of antidromic activation. The mean spontaneous discharge rate was significantly lower in the EB-treated than in the PG-treated OVX animals. In both groups, the activity of the majority (86% in the PG-treated animals and 88% in the EB-treated animals) of identified SFO neurons were activated by microiontophoretic application of angiotensin II (ANG II). Electrical stimulation of the lateral hypothalamic area (LHA) increased the excitability of these ANG II-sensitive SFO neurons (58% in the PG-treated animals and 52% in the EB-treated animals). The excitatory response to either ANG II or LHA stimulation was blocked by microiontophoretic application of the ANG II antagonist saralasin (Sar), suggesting that the excitatory response to LHA stimulation may be mediated by angiotensinergic LHA projections to the SFO. The magnitude of excitatory response to either ANG II or the LHA stimulation was much greater in the PG-treated than in the EB-treated animals. These results suggest that estrogen decreases the responsiveness of SFO neurons projecting to the PVN to angiotensinergic inputs from the LHA.
authors.affiliation: Department of Human Development, Naruto University of Education, Naruto, Tokushima, 772-8502, Japan. tanakaj@naruto-u.ac.jp
authors.forename: J
authors.initials: J
authors.lastname: Tanaka
authors.forename: H
authors.initials: H
authors.lastname: Miyakubo
authors.forename: M
authors.initials: M
authors.lastname: Nomura
mesh_terms: D000804:Angiotensin II / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D000818:Animals; D004958:Estradiol / Q000494:pharmacology; D004967:Estrogens / Q000494:pharmacology*; D005260:Female; D007026:Hypothalamic Area, Lateral / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D010052:Ovariectomy; D051381:Rats; D017208:Rats, Wistar; D012504:Saralasin / Q000494:pharmacology*; D012965:Sodium Chloride / Q000494:pharmacology; D013356:Subfornical Organ / Q000187:drug effects / Q000502:physiology*
chemical_list: D004967:Estrogens; D000804:Angiotensin II; D012965:Sodium Chloride; D004958:Estradiol; D012504:Saralasin