Immunohistochemical Investigation of the Magnocellular Peptidergic Hypothalamo-Neurohypophysial System of the Rat Chronically Stimulated by Long-Term Administration of Hypertonic Saline

Hd, Dellmann; Em, Rodríguez; Peña, P.; Siegmund, Inés

doi:10.1159/000124934

Cited by 17 publications

(6 citation statements)

References 22 publications

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“…These studies, however, employed uninephrectomized rats offered salt drinking only. In our opinion, they are not suitable models to study the role of mineralocorticoids on AVP mRNA expression because salt drinking alone as well as dehydration due to hypertonicity markedly increase AVP and OT mRNA levels and affect the immunoreactive AVP peptide content in the absence of administered mineralocorticoid [24, 36]. In agreement with these authors, we also found increased mRNA for AVP in the PVN from rats drinking 3% NaCl only but not receiving DOCA.…”

Section: Discussionsupporting

confidence: 88%

Increased Expression of Magnocellular Vasopressin mRNA in Rats with Deoxycorticosterone-Acetate Induced Salt Appetite

et al. 1998

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The neuropeptides arginine vasopressin (AVP) and oxytocin (OT) have been implicated in the genesis of hypertension due to deoxycorticosterone acetate (DOCA)-salt treatment of uninephrectomized rats. In this work, we studied if DOCA treatment of intact rats in doses arousing a salt appetite (a prehypertensive state), modulated mRNA for AVP and OT in the hypothalamus. Male Sprague-Dawley rats were offered both tap water and 3% NaCl in separate bottles and received vehicle or subcutaneous injections of 10 mg DOCA on alternate days for 7 days (4 injections) or 17 days (9 injections). They developed a preference for 3% NaCl solutions 24–48 h after treatment. Brain slices from rats killed on the 8th or 18th day were exposed to ³⁵S-labeled probes encoding prepro-AVP mRNA or OT mRNA, respectively. Expression of these mRNAs was measured in the magnocellular and parvocellular divisions of the paraventricular nucleus (PVN) and magnocellular cells of the supraoptic nucleus (SON). No changes were obtained in neuropeptide mRNA levels in the parvocellular division of the PVN between control and the two groups of DOCA-treated rats. However, DOCA-treated animals presented an increased number of grains per cell for AVP mRNA in the magnocellular division of the PVN and in magnocellular cells of the SON, as shown by group mean comparisons and frequency histograms. No changes were detected for OT mRNA. In a second series of studies, control or DOCA-treated rats were offered 3% NaCl or water as the only choice. Animals drinking 3% NaCl showed increased AVP and OT mRNA levels, whether they received DOCA or not. However, AVP mRNA levels in both nuclei were higher in DOCA-treated rats drinking 3% NaCl than in controls drinking salt solution. In comparison, control and DOCA-treated rats drinking water showed lower levels of AVP mRNA. OT mRNA levels in the SON remained unchanged in the same groups. The results suggest that in the magnocellular cells of the PVN and SON, increments in AVP mRNA are obtained following increments in salt intake produced by either mineralocorticoid treatment or exclusive salt drinking. In rats offered salt solution and water to drink, DOCA effects on AVP mRNA developed before changes occurred in serum sodium levels. Because combined DOCA + salt treatment induced a higher response in terms of AVP mRNA expression, we suggest that AVP could be a target of the central effects of the mineralocorticoid.

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Section: Discussionsupporting

confidence: 88%

Increased Expression of Magnocellular Vasopressin mRNA in Rats with Deoxycorticosterone-Acetate Induced Salt Appetite

et al. 1998

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“…Previous studies have reported activation of magnocellular OT neurons and parvocellular CRH neurons in the PVN under hyperosmotic conditions (Lightman & Young, 1987; Van Tol et al. , 1987; Dellmann et al. , 1988; Carter & Murphy, 1989; Amaya et al.…”

Section: Discussionmentioning

confidence: 98%

Up‐regulation of VGLUT2 expression in hypothalamic‐neurohypophysial neurons of the rat following osmotic challenge

Kawasaki

Hoshi²,

Kawano³

et al. 2005

Eur J of Neuroscience

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A second vesicular glutamate transporter (VGLUT2) has been reported to be expressed in neurosecretory neurons of the hypothalamic‐neurohypophysial system. To study its role in the neurosecretory neurons, we evaluated the expression of the VGLUT2 gene in the paraventricular (PVN) and supraoptic (SON) nuclei as well as the immunoreactivity in the neurohypophysis under euhydrated and chronic hyperosmotic conditions with in situ hybridization and immunohistochemistry. The intensity of hybridization signals in the PVN, SON and thalamus of rats subjected to water deprivation for 7 days, or drinking 2% NaCl for 4 or 7 days, was compared with that of euhydrated rats (control). The overall intensity in the entire PVN or SON, but not the thalamus, was higher in osmotically stimulated rats than in controls. Within the PVN, a significantly higher intensity of signals than that of controls was found only in the dorsolateral posterior magnocellular region in 4‐day salt‐loaded rats and in all subregions in water‐deprived or 7‐day salt‐loaded rats. The intensity in the SON was higher in the stimulated rats than in controls, regardless of subregions. In the neurohypophysis, VGLUT2 staining was frequently localized in vasopressin terminals of control rats and was apparently reduced in stimulated rats. These results indicate that VGLUT2 is principally expressed in magnocellular vasopressin neurons, suggesting some local effect of intrinsic glutamate on neurohypophysial hormone secretion.

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“…Here, we also report a decrease in 10% w/v sucrose intake in ad libitum fed and watered rats treated centrally with AM. OT has been described as a general satiety factor , Lokrantz et al 1997, Blevins et al 2004 and has also been shown to inhibit food , Sclafani et al 2007, water (Verty et al 2004), salt (Dellmann et al 1988, Blackburn et al 1992a,b, 1993, Murphy & Samson 1995, Allen et al 1997, and sucrose intakes among others (Lokrantz et al 1997, Sclafani et al 2007. If central AM is, indeed, activating OT neurons as we hypothesize, then the effects of AM should not be specific but rather AM would be a satiation cue for all ingestive behaviors.…”

Section: Discussionmentioning

confidence: 67%

“…Salt loading an animal will lead to significant increases in tissue Ot mRNA levels and plasma OT concentrations (Balment et al 1980, Van Tol et al 1987, Dellmann et al 1988, Verbalis & Dohinics 1991, Ozaki et al 2004. The effects of altered central AM levels on hypertonic saline-stimulated plasma OT levels were evaluated.…”

Section: Discussionmentioning

confidence: 99%

“…Chronic salt loading by increasing sodium intake in the diet led to increased Ot (listed as Oxt in the MGI Database) mRNA in the PVN and SON (Van Tol et al 1987, Dellmann et al 1988, Ozaki et al 2004). In addition, it appeared that there was a decrease in immunoreactive OT in the terminals of SON and PVN neurons, suggesting that more OT was being released into plasma and CNS sites (Dellmann et al 1988). Indeed, i.v.…”

Section: Introductionmentioning

confidence: 99%

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A possible relationship between brain-derived adrenomedullin and oxytocin in the regulation of sodium balance

White

Samson

2009

Journal of Endocrinology

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Exaggerated thirst and salt appetite occurs when endogenous, brain-derived adrenomedullin (AM) production is compromised. In addition, the arginine vasopressin (AVP) response to hypovolemia is compromised. We hypothesized that AM acts in the hypothalamus to control oxytocin (OT) release and that the inhibitory action of AM on salt appetite is mediated via its effects on OT release in the rat. When plasma tonicity was elevated with sodium, ribozymeinduced compromise of central AM production significantly blunted the release of OT into plasma. OT responses to elevation of plasma osmolality without concomitant change in plasma sodium levels were not altered by compromise of AM production. Thus, brain-derived AM controls OT release in response to altered plasma sodium levels.Furthermore, central AM-induced inhibition of NaCl intake can be reversed by pretreatment with an OT antagonist, and the increase in NaCl appetite seen following ribozyme compromise of central AM can be attenuated with central OT administration. These data support the hypothesis that endogenous, brain-derived AM is an essential participant in the hypothalamic response to hypernatremia via its actions on OT-expressing neurons. Together with our previous reports of the effects of AM on AVP secretion and ingestive behaviors, our results suggest that endogenous AM is a physiologically relevant regulator of the endocrine and behavioral mechanisms that maintain fluid and electrolyte homeostasis.

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Immunohistochemical Investigation of the Magnocellular Peptidergic Hypothalamo-Neurohypophysial System of the Rat Chronically Stimulated by Long-Term Administration of Hypertonic Saline

Cited by 17 publications

References 22 publications

Increased Expression of Magnocellular Vasopressin mRNA in Rats with Deoxycorticosterone-Acetate Induced Salt Appetite

Increased Expression of Magnocellular Vasopressin mRNA in Rats with Deoxycorticosterone-Acetate Induced Salt Appetite

Up‐regulation of VGLUT2 expression in hypothalamic‐neurohypophysial neurons of the rat following osmotic challenge

A possible relationship between brain-derived adrenomedullin and oxytocin in the regulation of sodium balance

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