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

Seth W Hurley; Zhongming Zhang; Terry G Beltz; Baojian Xue; Alan Kim Johnson

doi:10.1152/ajpregu.00210.2014

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

Journal article

Open access

Peer reviewed

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

Seth W Hurley, Zhongming Zhang, Terry G Beltz, Baojian Xue and Alan Kim Johnson

American journal of physiology. Regulatory, integrative and comparative physiology, Vol.307(12), pp.R1405-R1412

12/15/2014

DOI: 10.1152/ajpregu.00210.2014

PMCID: PMC4269674

PMID: 25354727

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Abstract

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.

Up-Regulation

Dehydration - chemically induced

Male

RNA, Messenger - metabolism

Dehydration - genetics

Time Factors

Behavior, Animal - drug effects

Dehydration - physiopathology

Hypothalamus - drug effects

Sodium, Dietary - metabolism

Disease Models, Animal

Dehydration - psychology

Captopril

Proto-Oncogene Proteins c-fos - metabolism

Appetite Regulation - drug effects

Renin-Angiotensin System - genetics

Hypothalamus - physiopathology

Rats, Sprague-Dawley

Furosemide

Animals

Hypothalamus - metabolism

Neuronal Plasticity

Renin-Angiotensin System - drug effects

Dizocilpine Maleate - pharmacology

Dehydration - metabolism

Details

Title: Subtitle: Sensitization of sodium appetite: evidence for sustained molecular changes in the lamina terminalis
Creators: Seth W Hurley - Department of Psychology, University of Iowa, Iowa City, Iowa
Zhongming Zhang - Department of Psychology, University of Iowa, Iowa City, Iowa; Nanyang Institute of Technology, Zhang Zhongjing College of Chinese Medicine, Nanyang, Henan Province, China
Terry G Beltz - Department of Psychology, University of Iowa, Iowa City, Iowa
Baojian Xue - Department of Psychology, University of Iowa, Iowa City, Iowa
Alan Kim Johnson - Department of Psychology, University of Iowa, Iowa City, Iowa; Department of Pharmacology, University of Iowa, Iowa City, Iowa; and Department of Health and Human Physiology, University of Iowa, Iowa City, Iowa; François M. Abboud Cardiovascular Center, University of Iowa, Iowa City, Iowa; and alan-johnson@uiowa.edu
Resource Type: Journal article
Publication Details: American journal of physiology. Regulatory, integrative and comparative physiology, Vol.307(12), pp.R1405-R1412
DOI: 10.1152/ajpregu.00210.2014
PMID: 25354727
PMCID: PMC4269674
NLM abbreviation: Am J Physiol Regul Integr Comp Physiol
ISSN: 0363-6119
eISSN: 1522-1490
Publisher: United States
Grant note: P01 HL014388 / NHLBI NIH HHS HL-098207 / NHLBI NIH HHS MH-08241 / NIMH NIH HHS R01 HL098207 / NHLBI NIH HHS HL-14388 / NHLBI NIH HHS
Language: English
Date published: 12/15/2014
Academic Unit: Psychological and Brain Sciences; Neuroscience and Pharmacology; Neurology (Pediatrics); Health, Sport, and Human Physiology
Record Identifier: 9984002437202771

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