Impaired Fluid Intake, but Not Sodium Appetite, in Aged Rats Is Mediated by the Cyclooxygenase-Prostaglandin E2 Pathway

Aging results in decreased fluid intake following dehydration and other dipsogenic stimuli; similar reductions in sodium intake have also been observed with aging. Given that cyclooxygenase (COX)-derived prostanoids are elevated in aged rats in the midbrain and proinflammatory prostanoids are known...

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Main Authors: Denovan P. Begg, Andrew J. Sinclair, Richard S. Weisinger
Format: Article
Language:English
Published: Frontiers Media S.A. 2020-02-01
Series:Frontiers in Aging Neuroscience
Subjects:
Online Access:https://www.frontiersin.org/article/10.3389/fnagi.2020.00019/full
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author Denovan P. Begg
Andrew J. Sinclair
Richard S. Weisinger
author_facet Denovan P. Begg
Andrew J. Sinclair
Richard S. Weisinger
author_sort Denovan P. Begg
collection DOAJ
description Aging results in decreased fluid intake following dehydration and other dipsogenic stimuli; similar reductions in sodium intake have also been observed with aging. Given that cyclooxygenase (COX)-derived prostanoids are elevated in aged rats in the midbrain and proinflammatory prostanoids are known to decrease fluid intake in dehydrated rats, the aim of this study was to determine if the reductions of fluid intake and sodium intake in aging are mediated by proinflammatory eicosanoid signaling. Therefore, we examined the effect of acute COX inhibition in adult (4 months-old) and aged (30 months-old) rats prior to ingestive behavior challenges. COX inhibition, using acetylsalicylic acid (ASA), increased fluid intake in aged, but not adult, rats in response to 24-h dehydration. ASA had no effect on salt intake following sodium depletion and ASA did not change basal fluid or sodium consumption in either age group. Hypothalamic COX-1 and -2, prostaglandin E synthase (PGES) and inducible nitric oxide synthase (iNOS) mRNA expression were all elevated in aged animals, leading to elevated PGE2 levels. COX expression in the hypothalamus was reduced by ASA treatment in rats of both ages resulting in reduced PGE2 levels in aged ASA treated animals. These data indicate that the reduced fluid intake that occurs in aging is due to increased COX-PGE2-mediated inflammation. However, the reduced sodium intake in these animals appears to occur via an alternate mechanism.
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spelling doaj.art-348ef6a99cf444199d9e02635c46caee2022-12-21T19:03:38ZengFrontiers Media S.A.Frontiers in Aging Neuroscience1663-43652020-02-011210.3389/fnagi.2020.00019488477Impaired Fluid Intake, but Not Sodium Appetite, in Aged Rats Is Mediated by the Cyclooxygenase-Prostaglandin E2 PathwayDenovan P. Begg0Andrew J. Sinclair1Richard S. Weisinger2School of Psychology, UNSW Sydney, Sydney, NSW, AustraliaFaculty of Health, Deakin University, Burwood, VIC, AustraliaSchool of Psychology, La Trobe University, Bundoora, VIC, AustraliaAging results in decreased fluid intake following dehydration and other dipsogenic stimuli; similar reductions in sodium intake have also been observed with aging. Given that cyclooxygenase (COX)-derived prostanoids are elevated in aged rats in the midbrain and proinflammatory prostanoids are known to decrease fluid intake in dehydrated rats, the aim of this study was to determine if the reductions of fluid intake and sodium intake in aging are mediated by proinflammatory eicosanoid signaling. Therefore, we examined the effect of acute COX inhibition in adult (4 months-old) and aged (30 months-old) rats prior to ingestive behavior challenges. COX inhibition, using acetylsalicylic acid (ASA), increased fluid intake in aged, but not adult, rats in response to 24-h dehydration. ASA had no effect on salt intake following sodium depletion and ASA did not change basal fluid or sodium consumption in either age group. Hypothalamic COX-1 and -2, prostaglandin E synthase (PGES) and inducible nitric oxide synthase (iNOS) mRNA expression were all elevated in aged animals, leading to elevated PGE2 levels. COX expression in the hypothalamus was reduced by ASA treatment in rats of both ages resulting in reduced PGE2 levels in aged ASA treated animals. These data indicate that the reduced fluid intake that occurs in aging is due to increased COX-PGE2-mediated inflammation. However, the reduced sodium intake in these animals appears to occur via an alternate mechanism.https://www.frontiersin.org/article/10.3389/fnagi.2020.00019/fullthirst and drinkingwater intakeagingsalt appetitesodium
spellingShingle Denovan P. Begg
Andrew J. Sinclair
Richard S. Weisinger
Impaired Fluid Intake, but Not Sodium Appetite, in Aged Rats Is Mediated by the Cyclooxygenase-Prostaglandin E2 Pathway
Frontiers in Aging Neuroscience
thirst and drinking
water intake
aging
salt appetite
sodium
title Impaired Fluid Intake, but Not Sodium Appetite, in Aged Rats Is Mediated by the Cyclooxygenase-Prostaglandin E2 Pathway
title_full Impaired Fluid Intake, but Not Sodium Appetite, in Aged Rats Is Mediated by the Cyclooxygenase-Prostaglandin E2 Pathway
title_fullStr Impaired Fluid Intake, but Not Sodium Appetite, in Aged Rats Is Mediated by the Cyclooxygenase-Prostaglandin E2 Pathway
title_full_unstemmed Impaired Fluid Intake, but Not Sodium Appetite, in Aged Rats Is Mediated by the Cyclooxygenase-Prostaglandin E2 Pathway
title_short Impaired Fluid Intake, but Not Sodium Appetite, in Aged Rats Is Mediated by the Cyclooxygenase-Prostaglandin E2 Pathway
title_sort impaired fluid intake but not sodium appetite in aged rats is mediated by the cyclooxygenase prostaglandin e2 pathway
topic thirst and drinking
water intake
aging
salt appetite
sodium
url https://www.frontiersin.org/article/10.3389/fnagi.2020.00019/full
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AT andrewjsinclair impairedfluidintakebutnotsodiumappetiteinagedratsismediatedbythecyclooxygenaseprostaglandine2pathway
AT richardsweisinger impairedfluidintakebutnotsodiumappetiteinagedratsismediatedbythecyclooxygenaseprostaglandine2pathway