Role of the lateral parabrachial nucleus in the control of sodium appetite

Jose V Menani; Laurival A De Luca Jr; Alan Kim Johnson

doi:10.1152/ajpregu.00251.2012

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Role of the lateral parabrachial nucleus in the control of sodium appetite

Journal article

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Peer reviewed

Role of the lateral parabrachial nucleus in the control of sodium appetite

Jose V Menani, Laurival A De Luca Jr and Alan Kim Johnson

American journal of physiology. Regulatory, integrative and comparative physiology, Vol.306(4), pp.R201-210

02/15/2014

DOI: 10.1152/ajpregu.00251.2012

PMCID: PMC3921312

PMID: 24401989

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Abstract

In states of sodium deficiency many animals seek and consume salty solutions to restore body fluid homeostasis. These behaviors reflect the presence of sodium appetite that is a manifestation of a pattern of central nervous system (CNS) activity with facilitatory and inhibitory components that are affected by several neurohumoral factors. The primary focus of this review is on one structure in this central system, the lateral parabrachial nucleus (LPBN). However, before turning to a more detailed discussion of the LPBN, a brief overview of body fluid balance-related body-to-brain signaling and the identification of the primary CNS structures and humoral factors involved in the control of sodium appetite is necessary. Angiotensin II, mineralocorticoids, and extracellular osmotic changes act on forebrain areas to facilitate sodium appetite and thirst. In the hindbrain, the LPBN functions as a key integrative node with an ascending output that exerts inhibitory influences on forebrain regions. A nonspecific or general deactivation of LPBN-associated inhibition by GABA or opioid agonists produces NaCl intake in euhydrated rats without any other treatment. Selective LPBN manipulation of other neurotransmitter systems [e.g., serotonin, cholecystokinin (CCK), corticotrophin-releasing factor (CRF), glutamate, ATP, or norepinephrine] greatly enhances NaCl intake when accompanied by additional treatments that induce either thirst or sodium appetite. The LPBN interacts with key forebrain areas that include the subfornical organ and central amygdala to determine sodium intake. To summarize, a model of LPBN inhibitory actions on forebrain facilitatory components for the control of sodium appetite is presented in this review.

Sodium, Dietary

Animals

Neural Inhibition

Prosencephalon - physiology

Appetite - physiology

Water-Electrolyte Balance

Neural Pathways - physiology

Rhombencephalon - physiology

Details

Title: Subtitle: Role of the lateral parabrachial nucleus in the control of sodium appetite
Creators: Jose V Menani - Department of Physiology and Pathology, School of Dentistry, Universidade Estadual Paulista, Araraquara, São Paulo, Brazil; and Departments of Psychology, Pharmacology and Health, and Human Physiology and the Cardiovascular Center, University of Iowa, Iowa City, Iowa
Laurival A De Luca Jr
Alan Kim Johnson
Resource Type: Journal article
Publication Details: American journal of physiology. Regulatory, integrative and comparative physiology, Vol.306(4), pp.R201-210
DOI: 10.1152/ajpregu.00251.2012
PMID: 24401989
PMCID: PMC3921312
NLM abbreviation: Am J Physiol Regul Integr Comp Physiol
ISSN: 0363-6119
eISSN: 1522-1490
Publisher: American Physiological Society; United States
Grant note: P01 HL014388 / NHLBI NIH HHS MH-80241 / NIMH NIH HHS HL-14388 / NHLBI NIH HHS HL-98207 / NHLBI NIH HHS
Language: English
Date published: 02/15/2014
Academic Unit: Psychological and Brain Sciences; Neuroscience and Pharmacology; Health, Sport, and Human Physiology
Record Identifier: 9984002592102771

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