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BS3 Chemical Crosslinking Assay: Evaluating the Effect of Chronic Stress on Cell Surface GABAA Receptor Presentation in the Rodent Brain
Published on: May 26, 2023
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Disruption of GluA2 phosphorylation potentiates stress responsivity.
Alexandra S Ellis1, Anne Q Fosnocht2, Kelsey E Lucerne3
1Department of Psychology, Temple University, United States; Neuroscience Program, Temple University, United States.
Behavioural Brain Research
|July 3, 2017
Summary
Disrupting GluA2 phosphorylation in mice increases vulnerability to stress-induced cocaine relapse and social avoidance. This highlights the GluA2 phosphorylation site as a potential target for stress-related disorders.
Area of Science:
- Neuroscience
- Molecular Biology
- Addiction Research
Background:
- Cocaine addiction involves persistent craving and relapse, often triggered by stress.
- Stress and cocaine use induce shared changes in synaptic plasticity, potentially explaining stress-induced relapse.
- Alterations in AMPA receptor trafficking, particularly GluA2 subunits, are implicated in these shared changes.
Purpose of the Study:
- To investigate the role of AMPA receptor trafficking in the interaction between stress and cocaine addiction.
- To examine stress responsivity in mice with disrupted PKC-mediated GluA2 phosphorylation.
Main Methods:
- Utilized a GluA2 K882A knock-in mouse model with disrupted PKC-mediated GluA2 phosphorylation.
- Assessed stress response following acute stress (forced swim) and after cocaine self-administration.
- Evaluated stress-induced reinstatement of cocaine seeking and conditioned reward.
- Measured social avoidance as an indicator of vulnerability to chronic social defeat stress.
Main Results:
- GluA2 K882A knock-in mice showed increased stress response after cocaine self-administration.
- Disrupted GluA2 phosphorylation heightened vulnerability to stress-induced reinstatement of cocaine seeking and reward.
- These mice also exhibited increased vulnerability to social defeat, indicated by greater social avoidance.
Conclusions:
- Disrupting GluA2 phosphorylation enhances responsivity to acute stress post-cocaine exposure.
- Impaired GluA2 phosphorylation increases vulnerability to both acute and chronic stress in the context of cocaine use.
- The GluA2 phosphorylation site represents a novel therapeutic target for stress-related disorders and addiction.
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