Differential effects of water and saline intake on water deprivation-induced c-Fos staining in the rat

Gottlieb, Helmut; Ji, Lianghui; Jones, Heath Gaedke; Penny, Maurice L.; Fleming, Tiffany; Cunningham, J. Thomas

doi:10.1152/ajpregu.00727.2005

Cited by 56 publications

(93 citation statements)

References 54 publications

(80 reference statements)

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“…shown to be upregulated in the SON after dehydration (Carter and Murphy, 1990;Sharp et al, 1991;Luckman et al, 1996;Miyata et al, 2001b;Cunningham et al, 2004;Ji et al, 2005;Kawasaki et al, 2005;Penny et al, 2005;Gottlieb et al, 2006). Here we identify JunD as also being upregulated (supplemental Table 3, available at www.jneurosci.org as supplemental material), an observation that we confirmed by in situ hybridization and immunocytochemistry (Yao et al, unpublished observation).…”

Section: Discussionsupporting

confidence: 81%

Transcription Factor Expression in the Hypothalamo-Neurohypophyseal System of the Dehydrated Rat: Upregulation of Gonadotrophin Inducible Transcription Factor 1 mRNA Is Mediated by cAMP-Dependent Protein Kinase A

Qiu¹,

Yao²,

Hindmarch³

et al. 2007

J. Neurosci.

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The supraoptic (SON) and paraventricular (PVN) nuclei of the hypothalamo-neurohypophyseal system (HNS) undergo a dramatic function-related plasticity during dehydration. We hypothesize that alterations in steady-state transcript levels might be partially responsible for this remodeling. In turn, regulation of transcript abundance might be mediated by transcription factors. We used microarrays to identify changes in the expression of mRNAs encoding transcription factors in response to water deprivation in the SON. We observed downregulation of 10 and upregulation of 28 transcription factor transcripts. For five of the upregulated mRNAs, namely gonadotropin inducible ovarian transcription factor 1 (Giot1), Giot2, cAMP-responsive element binding protein 3-like 1, CCAAT/enhancer binding protein ␤, and activating transcription factor 4, in situ hybridization was used to confirm the array results, demonstrating a significant increase in expression in SON and PVN magnocellular neurons (MCNs) after 3 d of water deprivation and, in some cases, upregulation in parvocellular PVN neurons. Using a viral vector expressing a potent inhibitor of cAMP-dependent protein kinase A (PKA), we show that the osmotically induced increase in the abundance of transcripts encoding Giot1 is mediated in vivo by the PKA pathway. We thus suggest that signaling pathways activated by dehydration in MCNs mediate transcription factor gene activation, which, in turn, regulate target genes that mediate HNS remodeling.

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Section: Discussionsupporting

confidence: 81%

Transcription Factor Expression in the Hypothalamo-Neurohypophyseal System of the Dehydrated Rat: Upregulation of Gonadotrophin Inducible Transcription Factor 1 mRNA Is Mediated by cAMP-Dependent Protein Kinase A

Qiu¹,

Yao²,

Hindmarch³

et al. 2007

J. Neurosci.

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“…Consequently, it was of interest to compare the pattern of activation in areas of brain after acute (2 h) or chronic (3 weeks) VNS. DFosB was measured to reflect chronic activation (Cunningham et al, 2007;Gottlieb et al, 2006;Herdegen and Leah, 1998;Ji et al, 2005;Nestler, 2004). There are four major protein members of the Fos family: c-Fos, FosB, Fra-1, and Fra-2 (Herdegen and Leah, 1998;Kovacs, 1998;Nestler, 2004).…”

Section: Discussionmentioning

confidence: 99%

Induction of c-Fos and ΔFosB Immunoreactivity in Rat Brain by Vagal Nerve Stimulation

Cunningham

Mifflin

Gould

et al. 2007

Neuropsychopharmacol

144

119

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Vagus nerve stimulation (VNS) is used as therapy for treatment-resistant depression or epilepsy. This study used immunohistochemistry for biomarkers of short-term (c-Fos) and long-term (DFosB) neuronal activation to map regions in brain that are activated by acute (2 h) or chronic (3 weeks) VNS in conscious Sprague-Dawley rats. Electrodes (Cyberonics Inc.) were implanted on the left vagus nerve and 1 week after surgery, stimulation began using parameters employed clinically (one burst of 20 Hz, 250 ms pulse width, 0.25 mA stimulation for 30 s every 5 min). Radio telemetry transmitters were used for monitoring blood pressure, heart rate, activity, and respiratory rate during VNS; neither acute nor chronic VNS significantly affected these parameters. Acute VNS significantly increased c-Fos staining in the nucleus of the solitary tract, paraventricular nucleus of the hypothalamus, parabrachial nucleus, ventral bed nucleus of the stria terminalis, and locus coeruleus but not in the cingulate cortex or dorsal raphe nucleus (DRN). Acute VNS did not affect DFosB staining in any region. Chronic VNS significantly increased DFosB and c-Fos staining bilaterally in each region affected by acute VNS as well as in the cingulate cortex and DRN. Using these stimulation parameters, VNS was tested for antidepressant-like activity using the forced swim test (FST). Both VNS and desipramine significantly decreased immobility in the FST; whereas desipramine decreased immobility by increasing climbing behavior, VNS did so by increasing swimming behavior. This study, then, identified potential sites in brain where VNS may produce its clinical effects.

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“…On the basis of previous reports, decapitation was deemed to be the most rapid and straightforward method to obtain the necessary size blood sample (4.4 ml) that was required for determination of plasma vasopressin and renin activity (19,23,60). Blood samples were collected in chilled centrifuge tubes containing ϳ10 l/ml EGTA (15%), sealed, and centrifuged at 5000 g for 10 min in a refrigerated centrifuge (internal temperature Ͻ4°C).…”

Section: Methodsmentioning

confidence: 99%

Regulation of plasma vasopressin and renin activity in conscious hindlimb-unloaded rats

Mueller¹,

Sullivan²,

Grindstaff³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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. Regulation of plasma vasopressin and renin activity in conscious hindlimb-unloaded rats. Am J Physiol Regul Integr Comp Physiol 291: R46 -R52, 2006. First published February 9, 2006 doi:10.1152/ajpregu.00622.2005.-Cardiovascular deconditioning occurs in astronauts after spaceflight or in individuals subjected to bed rest. It is characterized by an increased incidence of orthostatic intolerance. The mechanisms responsible for orthostatic intolerance are likely multifactorial and may include hypovolemia, autonomic dysfunction, and vascular and cardiac alterations. The arterial baroreflex is an important compensatory mechanism in the response to an orthostatic stress. In a previous study, we demonstrated that arterial baroreflex mediated sympathoexcitation was blunted in hindlimb-unloaded (HU) rats, a model of cardiovascular deconditioning. The arterial baroreflex also contributes to the regulation of vasoactive hormones including vasopressin and angiotensin II. In the present study, we tested the hypothesis that the neurohumoral response to hypotension is also attenuated in rats after 14 days of hindlimb unloading. To test this hypothesis, the vasodilator diazoxide (15 or 25 mg/kg) or saline (0.9%) was administered to produce hypotension or control conditions, respectively, in conscious HU and control rats. Plasma samples were collected and assayed for vasopressin and plasma renin activity (PRA). Diazoxide (25 mg/kg) produced significant increases in vasopressin and PRA compared with saline controls. HU rats exhibited significantly higher levels of vasopressin at rest and the increase in vasopressin levels during hypotension was enhanced by hindlimb unloading. Neither resting nor hypotension-induced PRA was altered by hindlimb unloading. These data suggest that although baroreflex-mediated sympathoexcitation is blunted by hindlimb unloading, hypotension-induced vasopressin release is enhanced and hypotension-induced PRA is unaffected. Increased circulating vasopressin may serve to compensate for blunted baroreflex regulation of sympathetic nervous activity produced by hindlimb unloading or may actually contribute to it. neurohumoral control; antidiuretic hormone; renin-angiotensin system ASTRONAUTS RETURNING FROM space, or individuals recovering from prolonged bed rest often experience symptoms of orthostatic intolerance (5,8,16,31,54,65). To delineate the possible mechanisms mediating orthostatic intolerance, individuals have been categorized as presyncopal or nonpresyncopal (17, 31, 66), finishers and nonfinishers (5), or simply, orthostatic tolerant and intolerant (54). No matter what nomenclature is used, the common characteristic among these individuals is an inability to maintain arterial pressure during an orthostatic challenge.Compensations for orthostatic stress include baroreflexmediated increases in heart rate in an attempt to maintain cardiac output, as well as increases in total peripheral resistance to maintain adequate arterial pressure (47). Initially, vasoconstriction is accomplished through a...

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Differential effects of water and saline intake on water deprivation-induced c-Fos staining in the rat

Cited by 56 publications

References 54 publications

Transcription Factor Expression in the Hypothalamo-Neurohypophyseal System of the Dehydrated Rat: Upregulation of Gonadotrophin Inducible Transcription Factor 1 mRNA Is Mediated by cAMP-Dependent Protein Kinase A

Transcription Factor Expression in the Hypothalamo-Neurohypophyseal System of the Dehydrated Rat: Upregulation of Gonadotrophin Inducible Transcription Factor 1 mRNA Is Mediated by cAMP-Dependent Protein Kinase A

Induction of c-Fos and ΔFosB Immunoreactivity in Rat Brain by Vagal Nerve Stimulation

Regulation of plasma vasopressin and renin activity in conscious hindlimb-unloaded rats

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