The transcription factor Phox2b is necessary for the development of the nucleus of the solitary tract (NTS). In this brainstem nucleus, Phox2b is expressed exclusively within a subpopulation of glutamatergic neurons. The present experiments in the adult rat were designed to test whether this subpopulation includes the aldosterone-sensitive NTS neurons, which express the enzyme 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2). Nuclear Phox2b was found in virtually all the HSD2 neurons (95-99%, n = 6 cases). Unlike the activity-related transcription factor c-Fos, Phox2b expression in the HSD2 neurons was not influenced by dietary sodium deprivation. The ubiquitous expression of Phox2b by the HSD2 neurons suggests that they are developmentally related to other Phox2b-dependent neurons of the NTS and that they release the excitatory neurotransmitter glutamate. This finding also suggests that human Phox2b mutations, which cause the central congenital hypoventilation syndrome (CCHS, also known as Ondine's curse), may also produce deficits in central aldosterone signaling and appetitive or autonomic responses to sodium deficiency.
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http://dx.doi.org/10.1016/j.brainres.2008.05.072 | DOI Listing |
J Comp Neurol
December 2024
Department of Neurology, University of Iowa, Iowa City, Iowa, USA.
Neuron
December 2024
Department of Physiology, University of California, San Francisco, San Francisco, CA 94158, USA; Kavli Center for Fundamental Neuroscience, University of California, San Francisco, San Francisco, CA 94158, USA; Neuroscience Graduate Program, University of California, San Francisco, San Francisco, CA 94158, USA; Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94158, USA. Electronic address:
JCI Insight
December 2024
Department of Neurology.
Mol Cell Endocrinol
October 2024
Department of Neuroscience and Pharmacology, University of Iowa, Iowa City, IA, USA; Iowa Neuroscience Institute, University of Iowa, Iowa City, IA, USA; Fraternal Order of Eagles Diabetes Research Center, University of Iowa, Iowa City, IA, USA; Interdisciplinary Graduate Program in Neuroscience, University of Iowa, Iowa City, IA, USA; Molecular Medicine Graduate Program, University of Iowa, Iowa City, IA, USA. Electronic address:
Mineralocorticoids play a key role in hydromineral balance by regulating sodium retention and potassium wasting. Through favoring sodium, mineralocorticoids can cause hypertension from fluid overload under conditions of hyperaldosteronism, such as aldosterone-secreting tumors. An often-overlooked mechanism by which aldosterone functions to increase sodium is through stimulation of salt appetite.
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January 2022
Department of Anesthesiology and Intensive Care Medicine, Charité Campus Benjamin Franklin, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität and Humboldt Universität zu Berlin, Berlin, Germany.
Recent interest has focused on the mineralocorticoid receptor (MR) and its impact on the myocardium and the performance of the heart. However, there is a lack of evidence about MR expression and its endogenous ligand aldosterone synthesis with specific regard to the intrinsic cardiac nervous system. Therefore, we looked for evidence of MR and aldosterone in sympathetic and parasympathetic neurons of intracardiac ganglia.
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