Body fluid homeostasis requires a complex suite of physiological and behavioral processes. Understanding of the role of the central nervous system (CNS) in integrating these processes has been advanced by research employing immunohistochemical techniques to assess responses to a variety of body fluid challenges. Such techniques have revealed sex/ @entity172 differences in CNS activation in response to @entity551 and @entity3489 . In contrast, it has been difficult to conclusively identify specific CNS areas and neurotransmitter systems that are activated by @entity2753 using these techniques. In part, this difficulty is due to the temporal disconnect between the physiological effects of treatments commonly used to deplete body @entity1372 and the behavioral response to such depletion. In some methods, @entity1372 ingestion is delayed in association with increased @entity398 (OT), suggesting an inhibitory role for OT in @entity1372 intake. Urinary @entity1372 loss increases within an hour after treatment with @entity1483 , a natriuretic-diuretic, but @entity1372 intake is delayed for 18-24h. Accordingly, we hypothesized that acute @entity1483 -induced @entity1372 loss activates centrally-projecting OT neurons which provide an initial inhibition of @entity1372 intake, and tested this hypothesis in ovariectomized @entity35 with or without @entity172 using immunohistochemical methods. Neuronal activation in the hypothalamic paraventricular nuclei (PVN) after administration of @entity1483 corresponded to the timing of the physiological effects. The activation was not different in @entity172 -treated @entity35 , nor did @entity172 alter the initial suppression of @entity1372 intake. However, virtually no fos immunoreactive (fos-IR) neurons in the parvocellular PVN were also immunolabeled for OT. Thus, acute @entity1372 loss after @entity1483 produces neural activation and an early inhibition of @entity1372 intake that does not appear to involve activation of centrally-projecting OT neurons and is not influenced by @entity172 .

Early XXXX inhibition of salt intake after @entity1483 treatment in @entity35 ?

@entity172 :: ('MESH:D004967', 'Chemical') :: ['estrogen'] @entity398 :: ('MESH:D010121', 'Chemical') :: ['oxytocin'] @entity1372 :: ('MESH:D012964', 'Chemical') :: ['sodium'] @entity1483 :: ('MESH:D005665', 'Chemical') :: ['furosemide'] @entity2753 :: ('MESH:D007010', 'Disease') :: ['hyponatremia'] @entity35 :: ('10116', 'Species') :: ['Sprague-Dawley rats', 'rats'] @entity551 :: ('MESH:D007022', 'Disease') :: ['hypotension'] @entity3489 :: ('MESH:D006955', 'Disease') :: ['hypernatremia']
@entity398 :: (MESH:D010121,Chemical) :: ['oxytocin']
