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mTORC1 in the orbitofrontal cortex promotes habitual alcohol seeking
Nadege Morisot1, Khanhky Phamluong1, Yann Ehinger1
1Department of Neurology, University of California, San Francisco, San Francisco, United States.
Elife
|December 11, 2019
Summary
Heavy alcohol use activates mTORC1 in the brain
Area of Science:
- Neuroscience
- Molecular Biology
- Addiction Research
Background:
- Mechanistic target of rapamycin complex 1 (mTORC1) is crucial for dendritic translation, learning, and memory.
- Previous research indicated heavy alcohol consumption activates mTORC1 in the rodent orbitofrontal cortex (OFC).
Purpose of the Study:
- To investigate the consequences of alcohol-induced mTORC1 activation in the OFC.
- To explore the role of the GluN2B/mTORC1 pathway in alcohol seeking and habit formation.
Main Methods:
- Inhibition of mTORC1 activity in the OFC of rats with habitual alcohol-seeking behavior.
- Inhibition of GluN2B in the OFC.
- Assessment of alcohol seeking and sensitivity to outcome devaluation.
- Comparison with habitual sucrose responding.
Main Results:
- mTORC1 inhibition in the OFC reduced alcohol seeking and restored outcome devaluation sensitivity in habitual alcohol-seeking rats.
- mTORC1 inhibition did not affect habitual sucrose responding, indicating specificity to alcohol.
- Inhibition of GluN2B in the OFC reduced alcohol-driven mTORC1 activation, alcohol seeking, and alcohol habit.
Conclusions:
- The GluN2B/mTORC1 signaling pathway in the OFC is a key driver of alcohol seeking and habit formation.
- Targeting this pathway may offer therapeutic strategies for alcohol use disorder.
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