Increased plasma osmolality by food intake evokes augmentation of plasma oxytocin (OT). Ovarian steroids may also influence the balance of body fluids by acting on OT neurones. Our aim was to determine if estrogen influences the activity of OT neurones in paraventricular nucleus (PVN) and supraoptic nucleus (SON) under different osmotic situations. Ovariectomized rats (OVX) were treated with either estradiol (E 2 ) or vehicle and were divided into three groups: group I was fed ad libitum, group II underwent 48 h of fasting, and group III was refed after 48 h of fasting. On the day of the experiment, blood samples were collected to determine the plasma osmolality and OT. The animals were subsequently perfused, and OT/FOS immunofluorescence analysis was conducted on neurones in the PVN and the SON. When compared to animals which were fasted or fed ad libitum, the plasma osmolality of refed animals was higher, regardless of whether they were treated with vehicle or E 2 . We observed neural activation of OT cells in vehicle-or E 2 -treated OVX rats refed after 48 h of fasting, but not in animals fed ad libitum or in animals that only underwent 48 h of fasting. Finally, the percentage of neurones that co-expressed OT and FOS was lower in both the PVN and the SON of animals treated with E 2 and refed, when compared to vehicle-treated animals. These results suggest that E 2 may have an inhibitory effect on OT neurones and may modulate the secretion of OT in response to the increase of osmolality induced by refeeding.
| INTRODUC TI ONVasopressin (AVP) secretion is a crucial neuroendocrine event for the maintenance of hydromineral homeostasis. 1,2 The two most prominent stimuli that lead to AVP secretion are hyperosmolality and hypovolaemia, comprising conditions that are induced by water deprivation (WD). AVP magnocellular neurones of the supraoptic (SON) and paraventricular (PVN) nuclei have the intrinsic capacity to respond to hyperosmolality. 3,4 This intrinsic osmosensitivity is related to the cell membrane properties of these neurones. The retraction of the cell volume that occurs as a result of hyperosmolality activates mechanosensitive cation channels, which, in these cells, specifically involve the TRPV (transient receptor potential vanilloid) channel, particularly the TRPV1 isoform. 3,5 In addition to this Vasopressinergic neurones of the supraoptic (SON) and paraventricular (PVN) nuclei express oestrogen receptor (ER)β and receive afferent projections from osmosensitive neurones that express ERα. However, which subtype of these receptors mediates the effects of oestradiol on vasopressin (AVP) secretion induced by hydromineral challenge has not yet been demonstrated in vivo. Moreover, AVP secretion induced by hyperosmolality is known to involve activation of TRPV1 (transient receptor potential vanilloid, member 1) in magnocellular neurones, although whether oestradiol modulates expression of this receptor is unknown. Thus, the present study aimed to clarify the mechanisms involved in the modulation exerted by oestradiol on AVP secretion, specifically investigating the involvement of ERβ, ERα and TRPV1 receptors in response to water deprivation (WD). We observed that treatment with an ERβ agonist potentiated AVP secretion and vasopressinergic neuronal activation induced by WD. This increase in AVP secretion induced by WD was reversed by an ERβ antagonist. By contrast to ERβ, the ERα agonist did not alter plasma AVP concentrations or activation of AVP neurones in the SON and PVN. Additionally, Fos expression in the subfornical organ was not altered by the ERα agonist. TRPV1 mRNA expression was increased by WD in the SON, although this response was not altered by any treatment. The results of the present study suggest that ERβ mediates the effects of oestradiol on AVP secretion in response to WD, indicating that the effects of oestradiol occur directly in AVP neurones without affecting TRPV1.
K E Y W O R D SERα, ERβ, TRPV1, vasopressin, water deprivation
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