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Modulation of Pathological Limbic Network Oscillations by Infralimbic Cortex Stimulation Correlates with Suppression of Opioid-Seeking Behavior
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1
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| Subject:
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Personalized Interventions and Diagnosis of Complex Neurological Disorders
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Presenter Author:
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| Name:
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Masoud Seddighfar
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Author:
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| Name 1:
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Masoud Seddighfar - Presenter
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| Affiliation 1:
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Neuroscience Research Center, Institute of Neuroscience and Cognition, Shahid Beheshti University of Medical Sciences, Tehran, Iran
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| Name 2:
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Zahra Bahmani
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| Affiliation 2:
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Department of Electrical & Computer Engineering, Tarbiat Modares University, Tehran.
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| Name 3:
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Abbas Haghparast - Corresponding
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| Affiliation 3:
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Neuroscience Research Center, Institute of Neuroscience and Cognition, Shahid Beheshti University of Medical Sciences, Tehran, Iran
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Abstract
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Original Research
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introduction :
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Relapse in opioid use disorder is driven by persistent, maladaptive neural adaptations, yet the specific network-level dynamics underlying this process remain poorly understood. The corticolimbic circuit, particularly the interplay between the basolateral amygdala (BLA) and ventral hippocampus (vHPC), is critical for addiction memory, but its electrophysiological signature during relapse is unclear. This study aimed to characterize the oscillatory dynamics of the BLA-vHPC network during morphine-seeking reinstatement and investigate how these dynamics are modulated by deep brain stimulation (DBS) of the infralimbic cortex (IL), a key region for inhibitory control.
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Methods:
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Local field potentials (LFPs) were recorded simultaneously from the BLA and vHPC in male Wistar rats during a morphine conditioned place preference (CPP) paradigm. We analyzed LFP power spectra and BLA-vHPC coherence during pre-conditioning, post-conditioning, extinction, and morphine-primed reinstatement. The effects of two IL DBS protocols—daily stimulation during extinction versus a single pre-reinstatement session—were assessed at high (130 Hz) and low (10 Hz) frequencies.
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Results:
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Morphine conditioning induced a distinct neural signature, altering power and coherence across multiple frequency bands. Critically, the reinstatement of drug-seeking behavior was robustly marked by the emergence of a pathological state of hypersynchrony, characterized by a significant and sharp increase in beta (12-30 Hz) and low-gamma (30-60 Hz) band coherence between the BLA and vHPC. The magnitude of this beta/low-gamma coherence was strongly and positively correlated with the behavioral expression of drug-seeking (R² > 0.55, P < 0.0001). Daily IL DBS, at both high and low frequencies, prevented the emergence of this reinstatement-associated hypersynchrony, suggesting the induction of lasting neuroplasticity. Furthermore, a single session of high-frequency DBS acutely suppressed this pathological coherence, an effect that was significantly weaker with low-frequency stimulation.
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Conclusion:
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These findings identify pathological beta-gamma hypersynchrony within the amygdala-hippocampal circuit as a robust, quantifiable neural signature of opioid relapse. The therapeutic efficacy of IL DBS is directly linked to its ability to prevent the network from entering this pathological state. This coherence pattern represents a promising electrophysiological biomarker for relapse and a direct target for developing and optimizing neuromodulation therapies for opioid use disorder.
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| Attachment:
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| Keywords:
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Deep Brain Stimulation (DBS), Reward and Addiction memory, Local Field Potential (LFP), Neural Coherence, Reinstatement, Morphine, Prefrontal Cortex, ventral Hippocampus, Basolateral Amygdala
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| Key message:
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