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      The Effect of High-Frequency Electrical Stimulation of Bilateral Nucleus Accumbens on the Behavior of Morphine-Induced Conditioned Place Preference Rats at Extinction and Reinstatement Phases

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          Abstract

          Objective

          To explore the optimal time points for deep brain stimulation (DBS) on the treatment of morphine addiction and its possible mechanisms by investigating how high-frequency stimulation (HFS) in bilateral nucleus accumbens (NAc) at different time points influences the addictive behaviors of rats with drug addiction.

          Methods

          The rats were randomly divided into extinction stimulation group ( n = 20) and postextinction stimulation group ( n = 20). Ten rats in the extinction stimulation group were treated using 120 Hz HFS during extinction stage while another 10 rats with pseudostimulation were served as control group. The CPP scores were evaluated at the second day after intervention, with total 9 sections accomplished. The CPP scores were evaluated at the second day of the intervention. In the postextinction stimulation group, 120 Hz HFS was intervened during the postextinction stage in 10 experimental rats and pseudostimulation was performed in 10 control rats. Stimulation was performed for 7 days continuously, and a small dose of morphine was administrated to induce relapse after the postextinction period.

          Results

          During the extinction phase, CPP scores after HFS were significantly higher. During the postextinction phase, relapse CPP scores after HFS were dramatically lower.

          Conclusion

          HFS of bilateral NAc inhibits the extinction of addictive behavior during the extinction phase, and HFS during the postextinction period suppresses relapse of drug seeking behavior.

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          Most cited references41

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          Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval.

          'New' memories are initially labile and sensitive to disruption before being consolidated into stable long-term memories. Much evidence indicates that this consolidation involves the synthesis of new proteins in neurons. The lateral and basal nuclei of the amygdala (LBA) are believed to be a site of memory storage in fear learning. Infusion of the protein synthesis inhibitor anisomycin into the LBA shortly after training prevents consolidation of fear memories. Here we show that consolidated fear memories, when reactivated during retrieval, return to a labile state in which infusion of anisomycin shortly after memory reactivation produces amnesia on later tests, regardless of whether reactivation was performed 1 or 14 days after conditioning. The same treatment with anisomycin, in the absence of memory reactivation, left memory intact. Consistent with a time-limited role for protein synthesis production in consolidation, delay of the infusion until six hours after memory reactivation produced no amnesia. Our data show that consolidated fear memories, when reactivated, return to a labile state that requires de novo protein synthesis for reconsolidation. These findings are not predicted by traditional theories of memory consolidation.
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            Probing and regulating dysfunctional circuits using deep brain stimulation.

            Despite the best available medical treatments, many patients continue to be disabled by neurologic and psychiatric disorders, resulting in a large unmet need. Advances in imaging and neurophysiology over the last two decades have led to a reinterpretation of some neurologic and psychiatric conditions as primarily disorders of circuit function, or "circuitopathies." These developments have been accompanied by advances in neurosurgical techniques with the increasingly widespread utilization of deep brain stimulation (DBS) to recalibrate dysfunctional circuits. The versatility of DBS as both a probe and modulator of neural circuits is making it a powerful tool to study the human brain, helping provide important details of the pathophysiology of circuit dysfunction. We are currently in a phase of active investigation to determine which circuits and disorders could be treated with DBS. Here we review recent advances in the DBS field and discuss potential future directions in targeted intracranial neuromodulation. Copyright © 2013 Elsevier Inc. All rights reserved.
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              Addiction: a disease of learning and memory.

              If neurobiology is ultimately to contribute to the development of successful treatments for drug addiction, researchers must discover the molecular mechanisms by which drug-seeking behaviors are consolidated into compulsive use, the mechanisms that underlie the long persistence of relapse risk, and the mechanisms by which drug-associated cues come to control behavior. Evidence at the molecular, cellular, systems, behavioral, and computational levels of analysis is converging to suggest the view that addiction represents a pathological usurpation of the neural mechanisms of learning and memory that under normal circumstances serve to shape survival behaviors related to the pursuit of rewards and the cues that predict them. The author summarizes the converging evidence in this area and highlights key questions that remain.
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                Author and article information

                Contributors
                Journal
                Evid Based Complement Alternat Med
                Evid Based Complement Alternat Med
                ECAM
                Evidence-based Complementary and Alternative Medicine : eCAM
                Hindawi
                1741-427X
                1741-4288
                2020
                12 October 2020
                12 October 2020
                : 2020
                : 8232809
                Affiliations
                Department of Neurosurgery, Changhai Hospital, Shanghai 200433, China
                Author notes

                Academic Editor: Ke Ren

                Author information
                https://orcid.org/0000-0002-1248-3420
                Article
                10.1155/2020/8232809
                7576340
                018ef497-d11e-46f7-ae45-39fc6a7d17c5
                Copyright © 2020 Chunhui Yang et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 6 March 2020
                : 25 August 2020
                : 21 September 2020
                Funding
                Funded by: National Natural Science Foundation of China
                Award ID: 81171296
                Funded by: National Key Research and Development Program
                Award ID: 2016YFC0105900
                Categories
                Research Article

                Complementary & Alternative medicine
                Complementary & Alternative medicine

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