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Related Experiment Videos

Sodium depletion and aldosterone decrease dopamine transporter activity in nucleus accumbens but not striatum.

M F Roitman1, T A Patterson, R R Sakai

  • 1Program in Neurobiology and Behavior, University of Washington, Seattle, Washington 98195, USA. roitman@u.washington.edu

The American Journal of Physiology
|May 8, 1999
PubMed
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Sodium depletion reduces dopamine transporter activity in the nucleus accumbens, potentially driving sodium appetite. Aldosterone directly impacts this dopamine transporter activity, influencing motivated behaviors.

Area of Science:

  • Neuroscience
  • Neuroendocrinology
  • Behavioral Neuroscience

Background:

  • Motivated behaviors, such as sodium appetite, are linked to increased dopamine (DA) transmission in the nucleus accumbens (NAc).
  • The dopamine transporter (DAT) regulates DA transmission and is implicated in motivated behaviors.
  • Sodium depletion reliably induces sodium appetite and is associated with changes in NAc DA transmission.

Purpose of the Study:

  • To investigate the role of the dopamine transporter (DAT) in the nucleus accumbens (NAc) during sodium appetite.
  • To determine if aldosterone (Aldo) directly affects DAT activity in the NAc.
  • To elucidate the mechanisms underlying increased NAc DA transmission during sodium appetite.

Main Methods:

  • In vivo sodium depletion in rats.

Related Experiment Videos

  • Rotating disk electrode voltammetry to measure DAT activity (Vmax of transport).
  • In vitro treatment with aldosterone (Aldo) to assess its direct effect on DAT activity.

    • Main Results:

    • Sodium depletion significantly decreased DAT activity in the rat NAc.
    • In vitro aldosterone treatment also reduced DAT activity in the NAc.
    • Neither sodium depletion nor aldosterone affected DAT activity in the striatum.

    Conclusions:

    • A direct action of aldosterone may contribute to the reduction in NAc DAT activity observed after sodium depletion.
    • Reduced DAT activity in the NAc could lead to increased DA transmission, potentially driving sodium appetite.
    • These findings suggest a neurobiological mechanism linking sodium balance, aldosterone, and motivated behavior.