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Prefrontal Neuronal Excitability Maintains Cocaine-Associated Memory During Retrieval
James M Otis1,2, Michael K Fitzgerald1, Hanna Yousuf1
1Department of Psychology, University of Wisconsin-Milwaukee, Milwaukee, WI, United States.
Frontiers in Behavioral Neuroscience
|July 3, 2018
Summary
Eliminating drug-associated memories may aid addiction recovery. This study found that inhibiting neuronal excitability in the prelimbic medial prefrontal cortex (PL-mPFC) during memory retrieval impairs cocaine-associated memories and prevents relapse.
Area of Science:
- Neuroscience
- Molecular Biology
- Addiction Research
Background:
- Drug-associated cues trigger craving and drug seeking, hindering addiction recovery.
- Memory retrieval makes emotionally salient memories vulnerable to disruption, potentially leading to long-lasting impairments.
- Noradrenergic signaling in the prelimbic medial prefrontal cortex (PL-mPFC) is implicated in maintaining drug-associated memories, but mechanisms are unclear.
Purpose of the Study:
- To investigate the physiological mechanisms underlying the maintenance of cocaine-associated memory during retrieval in rats.
- To determine if increased intrinsic neuronal excitability in the PL-mPFC contributes to the retrieval of cocaine-associated memories.
- To explore the role of cAMP-dependent signaling in maintaining these memories and its potential as a therapeutic target.
Main Methods:
- Combined *ex vivo* patch-clamp electrophysiology and *in vivo* behavioral neuropharmacology in rats.
- Assessed the impact of inhibiting noradrenergic beta-receptors in the PL-mPFC on cocaine-induced reinstatement.
- Investigated the effect of blocking a cAMP-dependent signaling cascade on memory retrieval and maintenance.
Main Results:
- Cocaine experience increases intrinsic excitability of pyramidal neurons in the PL-mPFC.
- This increased intrinsic plasticity predicts the retrieval of cocaine-associated memory (conditioned place preference).
- Pharmacological blockade of cAMP-dependent signaling during retrieval is necessary for memory maintenance and prevents subsequent cocaine-induced reinstatement.
Conclusions:
- Intrinsic neuronal excitability in the PL-mPFC is crucial for maintaining cocaine-associated memories during retrieval.
- Targeting PL-mPFC neuronal excitability during memory retrieval offers a potential strategy for eliminating drug-associated memories.
- This approach may provide a novel mechanism for addiction treatment by disrupting memory reconsolidation.
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