Subfornical organ connectivity and drinking to captopril or carbachol in rats.

Masson, Douglas B.; Fitts, Douglas A.

doi:10.1037/h0092456

Cited by 38 publications

(34 citation statements)

References 38 publications

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“…Extracellular dehydration was induced by subcutaneous injection of furosemide (10 mg/kg; Hospirca Lake Forest, IL) along with the antihypertensive drug captopril (5 mg/kg; Sigma Aldrich, St. Louis, MO), which results in a slight drop in blood pressure (ϳ10 mmHg) (31,50). Water was offered immediately after furo/cap treatment and 90 min later 1.8% NaCl access was added.…”

Section: Subjectsmentioning

confidence: 99%

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Sensitization of sodium appetite: evidence for sustained molecular changes in the lamina terminalis

Hurley

Zhang

Beltz

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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Animals with a history of sodium depletions exhibit increases in salt intake, a phenomenon described as the sensitization of sodium appetite. Using a novel experimental design, the present experiments investigated whether putative molecular markers of neural plasticity and changes in the message for components of the brain renin-angiotensin-aldosterone-system (RAAS) accompany the sensitization of sodium appetite. An initial set of experiments examined whether the glutamatergic N-methyl-d-aspartate receptor antagonist MK-801 would attenuate sodium appetite sensitization and prevent changes in mRNA expression associated with sensitization. Rats with repeated sodium depletions exhibited enhanced sodium appetite and mRNA expression for components of the RAAS in areas along the lamina terminalis (LT), a region of the brain that is important for the regulation of body fluid homeostasis, and these effects were significantly attenuated by MK-801 pretreatment. A second set of experiments investigated whether successive sodium depletions would elevate sodium intake and induce a pattern of fos-B staining consistent with the Δfos-B isoform in areas along the LT. The pattern of fos-B staining in the subfornical organ was consistent with the characteristics of Δfos-B expression. Specifically, fos-B/Δfos-B expression was increased 4 days after the last of a series of sodium depletions, fos-B/Δfos-B expression was nearly absent in control rats, and the quantity of fos-B/Δfos-B staining was directly associated with a history of sodium depletions. These findings demonstrate that the sensitization of sodium appetite is associated with sustained molecular alterations in the LT that are indicative of neural plasticity and upregulation of the central RAAS.

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Section: Subjectsmentioning

confidence: 99%

“…Coadministration of the diuretic furosemide along with the antihypertensive drug captopril (furo/cap) causes an extracellular dehydration concomitant with a slight drop in blood pressure (31,50). These effects result in a rapid onset of thirst and sodium appetite with a latency of ϳ1 h (17,31,50).…”

mentioning

confidence: 99%

Sensitization of sodium appetite: evidence for sustained molecular changes in the lamina terminalis

Hurley

Zhang

Beltz

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Consistent with this idea, Kisley and colleagues showed that pharmacological disruption of the genomic effects of estrogens reverses the attenuation of water intake stimulated by central administration of AngII [28]. Moreover, estradiol treatment reduces AngII receptor binding [27] and AngII receptor gene expression [32] in the subfornical organ (SFO), a forebrain circumventricular organ strongly implicated in drinking elicited by AngII [17,33,38]. Estradiol treatment also decreases isoproterenol-induced neuronal activation in the SFO [32].…”

Section: Introductionmentioning

confidence: 99%

Time course of behavioral, physiological, and morphological changes after estradiol treatment of ovariectomized rats

Graves

Hayes

Fan

et al. 2011

Physiology & Behavior

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Previous studies showed that treatment with 17-β-estradiol-3-benzoate (EB) reduces isoproterenol (ISOP) stimulated water intake by ovariectomized rats. This effect was observed 48 h after the second of two EB injections, suggesting that the attenuation is attributable to classic EB actions to alter gene expression. However, in addition to classic, slowly-occurring, genomic effects, estrogens have more rapidly-occurring effects that may be nongenomic or ‘nonclassical’ genomic effects. Thus, it is possible that the EB attenuation of water intake stimulated by ISOP is genomic, nongenomic, or both. Accordingly, we measured ISOP-induced water intake by OVX rats at different times after EB injections, using time points likely to indicate classic genomic effects (48 h or 24 h) or nonclassical genomic or nongenomic effects (90 min). We also examined EB effects on body weight, uterine weight, and plasma volume and Na+ concentration in the same animals using the same time points and EB dose. EB treatment decreased water intake stimulated by ISOP in both the 24-h and 48-h groups; however, water intake in the 90-min group was not affected by EB. Uterine weight was unchanged 90 min after EB, but was increased 24 h after the first injection of EB. In contrast, body weight decreased after EB, but not until 48 h after the second EB injection. Finally, EB did not alter plasma Na+ concentration or hematocrit, though plasma protein concentration increased transiently 24 h after EB treatment. Taken together, these findings suggest that the behavioral, morphological, and physiological effects of EB likely are attributable to slowly-occurring, classic genomic actions of estrogens. Moreover, the time course of the observed effects varied, suggesting tissue-specific differences in estrogen receptor density or subtype, or in co-activators or co-repressors that, ultimately, determine the timing and direction of EB effects.

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“…The present study uses the expression of Fos-ir to map areas of the rat forebrain and hindbrain that become metabolically active in a protocol that stimulates thirst and salt appetite within a 3-h experimental period (8,16,33,34). In this procedure, animals are made hypovolemic by administration of a diuretic (i.e., furosemide).…”

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confidence: 99%

Fos expression in rat brain during depletion-induced thirst and salt appetite

Thunhorst

Cicha

et al. 1998

American Journal of Physiology-Regulatory, Integrative and Comp

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The expression of Fos protein (Fos immunoreactivity, Fos-ir) was mapped in the brain of rats subjected to an angiotensin-dependent model of thirst and salt appetite. The physiological state associated with water and sodium ingestion was produced by the concurrent subcutaneous administration of the diuretic furosemide (10 mg/kg) and a low dose of the angiotensin-converting enzyme (ACE) inhibitor captopril (5 mg/kg; Furo/Cap treatment). The animals were killed 2 h posttreatment, and the brains were processed for Fos-ir to assess neural activation. Furo/Cap treatment significantly increased Fos-ir density above baseline levels both in structures of the lamina terminalis and hypothalamus known to mediate the actions of ANG II and in hindbrain regions associated with blood volume and pressure regulation. Furo/Cap treatment also typically increased Fos-ir density in these structures above levels observed after administration of furosemide or captopril separately. Fos-ir was reduced to a greater extent in forebrain than in hindbrain areas by a dose of captopril (100 mg/kg sc) known to block the actions of ACE in the brain. The present work provides further evidence that areas of lamina terminalis subserve angiotensin-dependent thirst and salt appetite.

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Subfornical organ connectivity and drinking to captopril or carbachol in rats.

Cited by 38 publications

References 38 publications

Sensitization of sodium appetite: evidence for sustained molecular changes in the lamina terminalis

Sensitization of sodium appetite: evidence for sustained molecular changes in the lamina terminalis

Time course of behavioral, physiological, and morphological changes after estradiol treatment of ovariectomized rats

Fos expression in rat brain during depletion-induced thirst and salt appetite

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