Mapping brain Fos immunoreactivity in response to water deprivation and partial rehydration: Influence of sodium intake.

Water deprivation (WD) followed by water intake to satiety, produces satiation of thirst and partial rehydration (PR). Thus, WD-PR is a natural method to differentiate thirst from sodium appetite. WD-PR also produces Fos immunoreactivity (Fos-ir) in interconnected areas of a brain circuit postulated to subserve sodium appetite. In the present work, we evaluated the effect of sodium intake on Fos-ir produced by WD-PR in brain areas operationally defined according to the literature as either facilitatory or inhibitory to sodium intake. Isotonic NaCl was available for ingestion in a sodium appetite test performed immediately after a single episode of WD-PR. Sodium intake decreased Fos-ir in facilitatory areas such as the lamina terminalis (particularly subfornical organ and median preoptic nucleus), central amygdala and hypothalamic parvocellular paraventricular nucleus in the forebrain. Sodium intake also decreased Fos-ir in inhibitory areas such as the area postrema, lateral parabrachial nucleus and nucleus of the solitary tract in the hindbrain. In contrast, sodium intake further increased Fos-ir that was activated by water deprivation in the dorsal raphe nucleus, another inhibitory area localized in the hindbrain. WD-PR increased Fos-ir in the core and shell of the nucleus accumbens. Sodium intake reduced Fos-ir in both parts of the accumbens. In summary, sodium intake following WD-PR reduced Fos-ir in most facilitatory and inhibitory areas, but increased Fos-ir in another inhibitory area. It also reduced Fos-ir in a reward area (accumbens). The results suggest a functional link between sodium intake and the activity of the hindbrain-forebrain circuitry subserving reward and sodium appetite in response to water deprivation.

Serotonergic system involvement in the inhibitory action of estrogen on induced sodium appetite in female rats.

This study of the participation of the serotonergic system in the inhibitory effect of estrogen on induced sodium appetite in female rats explores sodium appetite induced by Furosemide and low sodium diet treatment (DEP) in normally cycling rats and in ovariectomized rats with and without estradiol replacement (OVX, OVX+E(2)). We also analyzed the neural activity of serotonergic neurons of the dorsal raphe nucleus (DRN) as well as the activity of other brain nuclei previously found to be involved in sodium and water balance in sodium depleted animals without access to the intake test. For this purpose, we examined the brain Fos, Fos-serotonin and Fos-vasopressin immunoreactivity patterns in diestrus (D), estrus (E), OVX and OVX+E(2) rats subjected to DEP. Female rats in E and OVX+E(2) exhibited a significant decrease in induced sodium intake compared with females in D and OVX. This estrogen-dependent inhibition on induced sodium appetite (approximately 50% reduction) can be correlated with changes in Fos activation observed in the organum vasculosum of the lamina terminalis (OVLT) and DRN, in response to sodium depletion. Given our previous observations in males, the expected sodium depletion-induced activity of the OVLT was found to be absent in OVX+E(2) females, while the usual inhibitory tonic activity of serotonergic neurons of the DRN, instead of decreasing after sodium depletion, increases or remains unchanged in OVX+E(2)-DEP and E-DEP females, respectively. Regarding urinary water and sodium excretion 3h after furosemide treatment, E-DEP and OVX+E(2)-DEP animals excreted smaller volumes of more highly concentrated urine than depleted D and OVX rats. Twenty hours after sodium depletion, the same groups of animals also showed a significant increase in the number of Fos-AVP immunoreactive neurons within the supraoptic nucleus, compared with D-DEP. In summary, our results demonstrate an estrogen-dependent inhibition of induced sodium appetite in normally cycling rats and ovariectomized animals with estradiol replacement, which may involve an interaction between excitatory neurons of the OVLT and inhibitory serotonergic cells of the DRN. The main finding is thus serotonergic system involvement as a possible mechanism in the inhibitory action of estrogen on induced sodium appetite.

Early maternal separation and chronic variable stress as adults differentially affect Fos expression in the anterodorsal thalami nuclei.

The present study examined the participation of the anterodorsal thalamic nuclei (ADTN) in mediating the long-term effects of early maternal separation on the stress/hypothalamic-pituitary-adrenal axis response of adult animals. The study measured Fos and glucocorticoid receptor immunoreactivity (GR-ir) in the ADTN of maternally separated female rats subsequently exposed to variable chronic stress. Maternal separation increased the number of neurons immunoreactive to Fos in the ADTN of chronically stressed adult rats. GR-ir was absent in the ADTN. Linking these results with previous endocrine evidence led the authors to propose a dual role of these nuclei. Maternal separation and chronic stress enhance the neuronal activity of the ADTN, nevertheless it is not regulated, at least directly, via GR.