HSD2 neurons in the hindbrain drive sodium appetite

Area of Science:

• Neuroscience
• Physiology
• Endocrinology

Background:

• Sodium depletion in animals leads to an appetite for sodium, even at aversive concentrations.
• The neural mechanisms underlying sodium appetite are not fully understood.

Purpose of the Study:

• To investigate the role of aldosterone-sensitive neurons expressing 11β-hydroxysteroid dehydrogenase type 2 (HSD2) in the nucleus of the solitary tract in driving sodium appetite.
• To determine if chemogenetic activation of these neurons is sufficient to induce sodium consumption.

Main Methods:

• Utilized chemogenetics to activate specific HSD2-positive neurons in the nucleus of the solitary tract in mice.
• Assessed sodium consumption independently of thirst and hunger cues.
• Investigated the necessity of these HSD2-positive neurons for sodium appetite expression.

Main Results:

• Chemogenetic activation of HSD2-expressing neurons in the nucleus of the solitary tract was sufficient to drive the consumption of sodium-containing solutions.
• This effect occurred independently of the animals' hydration or satiety status.
• These HSD2-positive neurons were found to be necessary for the complete manifestation of sodium appetite.

Conclusions:

• Aldosterone-sensitive HSD2-expressing neurons in the nucleus of the solitary tract play a critical role in regulating sodium appetite.
• Activation of these neurons can independently drive sodium intake, suggesting a dedicated neural pathway for salt craving.
• Further research into the distinct downstream targets of these neurons may reveal novel insights into sodium homeostasis.