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Electrolytic lesions of the medial nucleus accumbens shell selectively decrease ethanol consumption without altering

Ronnie Dhaher¹, Deborah A Finn, Denesa L Oberbeck

¹Department of Behavioral Neuroscience, Oregon Health and Science University, Portland, OR 97239, United States. dhaherr@iupui.edu

Pharmacology, Biochemistry, and Behavior

|April 9, 2009

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The medial nucleus accumbens shell (MNAc shell) is crucial for limited access ethanol consumption in mice. Lesioning this brain region reduced alcohol intake but did not affect sucrose or free access consumption.

Area of Science:

Neuroscience
Behavioral Neuroscience
Addiction Research

Background:

The central extended amygdala (cExtA) is implicated in addiction.
The medial nucleus accumbens shell (MNAc shell) is part of the cExtA.
Understanding MNAc shell function is key to addiction research.

Purpose of the Study:

To investigate the MNAc shell's role in ethanol and sucrose consumption.
To differentiate MNAc shell involvement in limited vs. free access conditions.

Main Methods:

Bilateral electrolytic lesions of the MNAc shell or sham surgery in C57BL/6J mice.
Limited access (2h) two-bottle choice ethanol and sucrose consumption tests.
Free access (24h) two-bottle choice ethanol consumption test.

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Main Results:

MNAc shell lesions significantly decreased ethanol consumption during limited access.
Sucrose consumption and free access ethanol consumption were not affected by MNAc shell lesions.
These findings highlight a specific role for the MNAc shell in limited alcohol intake.

Conclusions:

The MNAc shell is a critical neural component for limited access alcohol consumption.
This region's involvement in alcohol consumption may be context-dependent (limited vs. free access).
Further research into MNAc shell circuitry could inform addiction treatment strategies.