4.5 Article

Aldosterone-sensitive neurons in the nucleus of the solitary tract: Bidirectional connections with the central nucleus of the amygdala

Journal

JOURNAL OF COMPARATIVE NEUROLOGY
Volume 497, Issue 4, Pages 646-657

Publisher

WILEY
DOI: 10.1002/cne.21019

Keywords

11-beta-hydroxysteroid dehydrogenase type 2; HSD2; 11HSD2; aldosterone; mineralocorticoid; nucleus tractus solitarius; NTS; sodium appetite; salt appetite; salt ingestion; ingestive behavior; central nucleus of the amygdala; conditioned taste aversion

Funding

  1. NHLBI NIH HHS [R01 HL025449, R01 HL025449-33A1, R37 HL025449, HL-25449] Funding Source: Medline

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The HSD2 (11-beta-hydroxysteroid dehydrogenase type 2-expressing) neurons in the nucleus of the solitary tract (NTS) of the rat are aldosterone-sensitive and have been implicated in sodium appetite. The central nucleus of the amygdala (CeA) has been shown to modulate salt intake in response to aldosterone, so we investigated the connections between these two sites. A prior retrograde tracing study revealed only a minor projection from the HSD2 neurons directly to the CeA, but these experiments suggested that a more substantial projection may be relayed through the parabrachial nucleus. Small injections of cholera toxin beta subunit (CTb) into the external lateral parabrachial subnucleus (PBel) produced both retrograde cell body labeling in the HSD2 neurons and anterograde axonal labeling in the lateral subdivision of the CeA. Also, injections of either CTb or Phaseolus uulgaris leucoagglutinin into the medial subdivision of the CeA labeled a descending projection from the amygdala to the medial NTS. Axons from the medial CeA formed numerous varicosities and terminals enveloping the HSD2 neurons. Complementary CTb injections, centered in the HSD2 subregion of the NTS, retrogradely labeled neurons in the medial CeA. These bidirectional projections could form a functional circuit between the HSD2 neurons and the CeA. The HSD2 neurons may represent one of the functional inputs to the lateral CeA, and their activity may be modulated by a return projection from the medial CeA. This circuit could provide a neuroanatomical basis for the modulation of salt intake by the CeA.

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