Fos expression following isotonic volume expansion  of the unanesthetized male rat

Randolph, R. R.; Li, Q.; Curtis, Kathleen S.; Sullivan, Margaret J.; Cunningham, J. Thomas

doi:10.1152/ajpregu.1998.274.5.r1345

Cited by 28 publications

(46 citation statements)

References 32 publications

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“…14) or 10 ml/100 g in 10 min (Ref. 32) compared with 1.5 or 3 ml/rat in 11 or 22 min, respectively, in the current study]. The infusions in our study were bracketed by 0.7-ml blood samples that would have mitigated their effect on blood volume.…”

Section: Discussionmentioning

confidence: 66%

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Differential effects of intravenous hyperosmotic solutes on drinking latency and c-Fos expression in the circumventricular organs and hypothalamus of the rat

Ho¹,

Zierath²,

Savos³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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December 28, 2006; doi:10.1152/ajpregu.00547.2006.-Hyperosmotic intravenous infusions of NaCl are more potent for inducing drinking and vasopressin (AVP) secretion than equally osmotic solutions of glucose or urea. The fact that all three solutes increased cerebrospinal fluid osmolality and sodium concentration led the investigators to conclude that critical sodium receptors or osmoreceptors for stimulating drinking and AVP secretion were outside the blood-brain barrier (BBB) in the circumventricular organs (CVOs). We tested an obvious prediction of this hypothesis: that all three solutes should increase c-Fos-like immunoreactivity (Fos-ir) inside the BBB, but that only NaCl should increase Fos-ir in the CVOs. We gave intravenous infusions of 3.0 Osm/l NaCl, glucose, or urea to rats for 11 or 22 min at 0.14 ml/min and perfused the rats for assay of Fos-ir at 90 min. Controls received isotonic NaCl at the same volume. Drinking latency was measured, but water was then removed. Drinking consistently occurred with short latency during hyperosmotic NaCl infusions only. Fos-ir in the forebrain CVOs, the subfornical organ, and organum vasculosum laminae terminalis was consistently elevated only by hyperosmotic NaCl. However, all three hyperosmotic solutes potently stimulated Fos-ir in the supraoptic and paraventricular nuclei of the hypothalamus inside the BBB. Hyperosmotic NaCl greatly elevated Fos-ir in the area postrema, but even glucose and urea caused moderate elevations that may be related to volume expansion rather than osmolality. The data provide strong support for the conclusion that the osmoreceptors controlling drinking are located in the CVOs. area postrema; c-Fos; drinking; hypernatremia; organum vasculosum laminae terminalis; osmoreceptors; paraventricular nucleus of the hypothalamus; subfornical organ; supraoptic nucleus THE BRAIN AREAS THAT CONTAIN electrophysiologically defined osmoreceptive cells that function in the regulation of fluid and electrolyte balance include the circumventricular organs (CVOs), the median preoptic nucleus (MnPO), the hypothalamic supraoptic and paraventricular nuclei (SON and PVN), and the nucleus of the solitary tract (1,17,18,33,34,40,43). These areas are intricately interconnected by neural pathways into a network subserving fluid balance as originally described by Miselis (29). Candidate mechanisms for osmoreceptors have been identified among aquaporins, the vanilloid family of transient receptor potential channels, and mechanical gating of sodium currents (3,22,44,45). However, electrophysiological studies in single neurons or brain slices do little to differentiate which osmoreceptors are more important for functions such as AVP secretion or drinking.The concept that the critical osmoreceptors for these functions are located in the CVOs and in the peripheral nervous system stems from three influential studies that demonstrated drinking in sheep, dogs, and rats was elicited by intravenous hyperosmotic NaCl or sucrose but not by urea or glucose (8,26,41). The generally...

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Section: Discussionmentioning

confidence: 66%

“…Volume expansion, rather than osmolality, in the hyperosmotic groups might also have contributed to some of the Fos-ir observed in the hypothalamus and AP (14,32). Studies of c-Fos expression after isotonic blood volume expansion used much larger volumes of infused fluid than we did [e.g., 2 ml/100 g in 60 s (Ref.…”

Section: Discussionmentioning

confidence: 84%

Differential effects of intravenous hyperosmotic solutes on drinking latency and c-Fos expression in the circumventricular organs and hypothalamus of the rat

Ho¹,

Zierath²,

Savos³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Within the brain stem, the portion of NTS analyzed was from 300 m caudal to obex extending rostrally 300 -400 m beyond the area postrema (53). This area corresponds to Ϫ13.2 to Ϫ14.6 mm posterior to bregma according to the atlas of Paxinos and Watson (47).…”

mentioning

confidence: 99%

Chronic intermittent hypoxia increases blood pressure and expression of FosB/ΔFosB in central autonomic regions

Knight

Little

Carreño

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

117

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Chronic intermittent hypoxia (CIH) models repetitive bouts of arterial hypoxemia that occur in humans suffering from obstructive sleep apnea. CIH has been linked to persistent activation of arterial chemoreceptors and the renin-angiotensin system, which have been linked to chronic elevations of sympathetic nerve activity (SNA) and mean arterial pressure (MAP). Because Fos and FosB are transcription factors involved in activator protein (AP)-1 driven central nervous system neuronal adaptations, this study determined if CIH causes increased Fos or FosB staining in brain regions that regulate SNA and autonomic function. Male Sprague Dawley rats were instrumented with telemetry transmitters for continuous recording of MAP and heart rate (HR). Rats were exposed to continuous normoxia (CON) or to CIH for 8 h/day for 7 days. CIH increased MAP by 7-10 mmHg without persistently affecting HR. A separate group of rats was killed 1 day after 7 days of CIH for immunohistochemistry. CIH did not increase Fos staining in any brain region examined. Staining for FosB/ΔFosB was increased in the organum vasculosum of the lamina terminalis (CON: 9 ± 1; CIH: 34 ± 3 cells/section), subfornical organ (CON: 7 ± 2; CIH: 31 ± 3), median preoptic nucleus (CON 15 ± 1; CIH: 38 ± 3), nucleus of the solitary tract (CON: 9 ± 2; CIH: 28 ± 4), A5 (CON: 3 ± 1; CIH: 10 ± 1), and rostral ventrolateral medulla (CON: 5 ± 1; CIH: 17 ± 2). In the paraventricular nucleus, FosB/ΔFosB staining was located mainly in the dorsal and medial parvocellular subnuclei. CIH did not increase FosB/ΔFosB staining in caudal ventrolateral medulla or supraoptic nucleus. These data indicate that CIH induces an increase in FosB/ΔFosB in autonomic nuclei and suggest that AP-1 transcriptional regulation may contribute to stable adaptive changes that support chronically elevated SNA.

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“…The CVLM was defined posteriorly by the pyramidal decussation and anteriorly by the appearance of the principle nucleus of the inferior olive. 30,31 The anterior border of the RVLM was defined by the caudal pole of the facial nucleus, and the rostral hypoglossal nucleus was used for the posterior border. 30,31 Analysis of the PBN included the ventral lateral, central medial, external lateral, and external medial regions, which included the pontine taste area.…”

Section: Fos Immunocytochemistrymentioning

confidence: 99%

“…30,31 The anterior border of the RVLM was defined by the caudal pole of the facial nucleus, and the rostral hypoglossal nucleus was used for the posterior border. 30,31 Analysis of the PBN included the ventral lateral, central medial, external lateral, and external medial regions, which included the pontine taste area. The numbers of Fos-positive cells in each region were tabulated for each section without knowledge of which treatment group the sections were from.…”

Section: Fos Immunocytochemistrymentioning

confidence: 99%

Identification of Active Central Nervous System Sites in Renal Wrap Hypertensive Rats

et al. 2007

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Abstract-To identify central neurons participating in cardiovascular regulation in hypertension, we studied Fos staining, a marker for synaptically activated neurons, in adult male normotensive and hypertensive (HT) rats. At 1 and 4 weeks after induction of unilateral nephrectomy, renal wrap hypertension mean arterial pressure was 138Ϯ4 mm Hg (nϭ6) in 1-week HT rats and 159Ϯ6 mm Hg (nϭ6) in 4-week HT rats. Mean arterial pressure was 103Ϯ2 mm Hg (nϭ6) in sham-operated, normotensive rats. Mean arterial pressure was greater in both HT groups compared with normotensive rats, and the mean arterial pressure in 4-week HT rats was greater than that in 1-week HT rats. Rats were anesthetized and perfused, brains sectioned and processed using a Fos antibody, and the number of Fos immunoreactive neurons counted in sections through various brain regions. Hypertension of 1 or 4 weeks did not alter the number of Fos immunoreactive neurons in the area postrema, the supraoptic nucleus, and the median preoptic nucleus. The number of Fos immunoreactive neurons was increased after 1 and 4 weeks in the nucleus of the solitary tract, both the caudal and ventral lateral medulla, and the organum vasculosum of the lamina terminalis. In addition, after 4 weeks of HT, the number of Fos immunoreactive neurons was increased in the parabrachial nucleus and the paraventricular nucleus of the hypothalamus. The results indicate central regions active in acute and chronic HT rats and suggest certain areas that may be differentially activated depending on the duration of the hypertension. Key Words: baroreceptor Ⅲ brain Ⅲ immunohistochemistry I mmunocytochemistry for the protein Fos has been widely used to map the activation of specific regions of the central nervous system associated with acute homeostatic challenges. [1][2][3][4] Fos is an immediate early gene transcription factor that has been shown to be present in synaptically activated cells. 5 A number of studies in the rat have examined areas in the central nervous system where neurons express Fos after brief increases in arterial blood pressure 6 -13 ; however, few studies have sought to identify which of these areas might be active in chronically hypertensive (HT) rats. 14 -17 At present, our current understanding of central nervous system function in hypertension is limited because of the lack of quantitative answers to fundamental questions. Many of these questions deal with the overall operating characteristics of the peripheral and central sites that regulate blood pressure. For example, is the number of neurons active in a particular brain region different in an HT compared with a normotensive (NT) individual? Is the number of neurons active in a particular brain region graded as a function of the magnitude or the duration of the change in blood pressure?Therefore, quantification of the number of neurons in key central sites active in renal wrap HT rats is important. Such information could provide insights into areas that are likely candidates to mediate the elevated sympathetic ...

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Fos expression following isotonic volume expansion of the unanesthetized male rat

Cited by 28 publications

References 32 publications

Differential effects of intravenous hyperosmotic solutes on drinking latency and c-Fos expression in the circumventricular organs and hypothalamus of the rat

Differential effects of intravenous hyperosmotic solutes on drinking latency and c-Fos expression in the circumventricular organs and hypothalamus of the rat

Chronic intermittent hypoxia increases blood pressure and expression of FosB/ΔFosB in central autonomic regions

Identification of Active Central Nervous System Sites in Renal Wrap Hypertensive Rats

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