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Simultaneous Detection of c-Fos Activation from Mesolimbic and Mesocortical Dopamine Reward Sites Following Naive Sugar and Fat Ingestion in Rats

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Parabrachial and hypothalamic interaction in sodium appetite.

S Dayawansa¹, S Peckins, S Ruch

¹Dept. of Neural and Behavioral Sciences, College of Medicine, The Pennsylvania State University, Milton S. Hershey Medical Center, Hershey, PA 17033-0850, USA.

American Journal of Physiology. Regulatory, Integrative and Comparative Physiology

|January 29, 2011

Summary

Rats with lateral hypothalamus or parabrachial nuclei damage lose sodium appetite. Asymmetric lesions confirm that communication between these brain areas is essential for salt appetite, dissociating it from weight loss.

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Area of Science:

Neuroscience
Behavioral Neuroscience

Background:

Bilateral lesions of the lateral hypothalamus (LH) or parabrachial nuclei (PBN) abolish sodium appetite in rats.
The PBN's projection to the LH is primarily ipsilateral, suggesting a potential functional dependency between these areas.

Purpose of the Study:

To investigate if functionally dependent deficits in sodium appetite result from asymmetric lesions affecting both the PBN and LH.
To dissociate the loss of sodium appetite from weight changes following LH damage.

Main Methods:

Rats received bilateral ibotenic acid lesions of the LH, which caused weight loss and eliminated sodium appetite.
Control rats with ipsilateral PBN and LH lesions maintained weight and showed normal sodium appetite.
Rats with asymmetric PBN-LH lesions gained weight but failed to increase sodium intake after depletion.

Main Results:

Asymmetric lesions of the PBN and LH blocked sodium appetite, similar to bilateral lesions.
Weight loss observed with bilateral LH lesions was not a prerequisite for the loss of sodium appetite.
Sodium appetite is dependent on communication between neurons in the LH and PBN.

Conclusions:

Sodium appetite requires intact communication between the lateral hypothalamus and the parabrachial nuclei.
The study dissociates the neural circuitry of sodium appetite from that controlling body weight regulation.