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A New Method for Inducing a Depression-Like Behavior in Rats
Published on: February 22, 2018
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Both Ketamine and NBQX Attenuate Alcohol-Withdrawal Induced Depression in Male Rats
Bruk Getachew1, Yousef Tizabi1
1Department of Pharmacology, Howard University College of Medicine, Washington, DC, USA.
Journal of Drug and Alcohol Research
|April 30, 2019
Summary
Ketamine and NBQX, targeting specific brain receptors, show potential for treating depression associated with alcohol withdrawal. These drugs may help normalize brain-derived neurotrophic factor (BDNF) levels, aiding alcohol cessation.
Area of Science:
- Neuroscience
- Pharmacology
- Addiction Research
Background:
- Co-occurring heavy drinking and depression impede alcohol cessation.
- Ketamine, an NMDA receptor antagonist, exhibits rapid antidepressant effects.
- Understanding mechanisms of alcohol withdrawal-induced depression is crucial for treatment.
Purpose of the Study:
- To investigate the efficacy of ketamine and NBQX in mitigating alcohol withdrawal-induced depression in a rat model.
- To explore the role of AMPA/kainate receptors in alcohol withdrawal-related depressive behaviors.
- To examine the impact of these antagonists on hippocampal brain-derived neurotrophic factor (BDNF) levels.
Main Methods:
- Adult male Wistar rats were subjected to chronic ethanol exposure to induce withdrawal.
- Animals received intraperitoneal injections of ketamine, NBQX, or a combination thereof.
- Behavioral tests (Open Field Locomotor Activity, Forced Swim Test) and hippocampal BDNF levels were assessed.
Main Results:
- Alcohol withdrawal increased immobility in the Forced Swim Test, indicating depressive-like behavior.
- Both ketamine and NBQX individually normalized the swimming behavior and restored hippocampal BDNF levels.
- Combined administration of ketamine and NBQX negated their individual therapeutic effects.
Conclusions:
- NMDA and AMPA/kainate receptor antagonists may offer therapeutic benefits for alcohol use disorder.
- The effects appear to be mediated, at least partially, through modulation of hippocampal BDNF.
- Further research into the combined use and precise mechanisms is warranted.
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