Intra-accumbal CB1 receptor blockade reduced extinction and reinstatement of morphine

Khaleghzadeh‐Ahangar, Hossein; Haghparast, Abbas

doi:10.1016/j.physbeh.2015.06.005

Cited by 31 publications

(22 citation statements)

References 37 publications

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“…and decreases reinstated heroin seeking (57,58). Akin to mGluR2/3, presynaptic cannabinoid CB 1 receptors regulate glutamate release probability, and intra-accumbens administration of AM251, a CB 1 receptor antagonist, diminishes the duration required to extinguish morphine conditioned place preference (CPP) as well as the duration of morphine-induced reinstatement of CPP (59). In addition, the CB 1 receptor antagonist AM4113 dose-dependently suppresses heroin selfadministration (60).…”

Section: Presynaptic Plasticitymentioning

confidence: 99%

The Opioid-Addicted Tetrapartite Synapse

Kruyer¹,

Chioma²,

Kalivas

2020

Biological Psychiatry

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Opioid administration in preclinical models induces long-lasting adaptations in reward and habit circuitry. The latest research demonstrates that in the nucleus accumbens, opioid-induced excitatory synaptic plasticity involves presynaptic and postsynaptic elements as well as adjacent astroglial processes and the perisynaptic extracellular matrix. We outline opioid-induced modifications within each component of the tetrapartite synapse and provide a neurobiological perspective on how these adaptations converge to produce addiction-related behaviors in rodent models. By incorporating changes observed at each of the excitatory synaptic compartments into a unified framework of opioid-induced glutamate dysregulation, we highlight new avenues for restoring synaptic homeostasis that might limit opioid craving and relapse vulnerability.

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Section: Presynaptic Plasticitymentioning

confidence: 99%

The Opioid-Addicted Tetrapartite Synapse

Kruyer¹,

Chioma²,

Kalivas

2020

Biological Psychiatry

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“…The NMDA receptor glycine site full agonist d ‐serine and the partial agonist d ‐cycloserine both have the ability to facilitate extinction and reduce the subsequent reinstatement of drug reward memory (Botreau et al ., ; Paolone et al ., ; Lu et al ., ; Hammond et al ., ; Kiefer et al ., ; Liu et al ., ; see Myers & Carlezon, ; for review). Moreover, microinjection of a CB1 receptor antagonist into the NAc before daily test sessions (extinction) facilitated the extinction and decreased the reinstatement after extinction of morphine CPP (Khaleghzadeh‐Ahangar & Haghparast, ). Other studies also investigated the effects of post‐extinction pharmacological interventions on the extinction of drug reward memory.…”

Section: Pharmacological Modulation Of Extinction Of Drug Reward Memorymentioning

confidence: 99%

“…A growing number of studies have demonstrated that the modulation of various receptors, such as NMDA receptors, a-amino-3hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors and cannabinoid type 1 (CB1) receptors, can facilitate the extinction of drug reward memory (Gass & Olive, 2009;Heinrichs et al, 2010;Khaleghzadeh-Ahangar & Haghparast, 2015;Chen et al, 2016). It was demonstrated that pre-extinction administration of the metabotropic glutamate receptor 5 (mGluR5)-positive allosteric modulator 3-cyano-N-(1,3-diphenyl-1H-pyrazol-5-yl)-benzamide (CDPPB) facilitated extinction of cocaine CPP, which was blocked by the mGluR5 antagonist MTEP or the NMDA antagonist MK-801 (Gass & Olive, 2009).…”

Section: Pharmacological Modulation Of Extinction Of Drug Reward Memorymentioning

confidence: 99%

Modulating reconsolidation and extinction to regulate drug reward memory

Liu

Tian

2018

Eur J of Neuroscience

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Drug addiction is an aberrant memory that shares the same memory processes as other memories. Brief exposure to drug-associated cues could result in reconsolidation, a hypothetical process during which original memory could be updated. In contrast, longer exposure times to drug-associated cues could trigger extinction, a process that decreases the conditioned responding. In this review, we discuss the pharmacological and non-pharmacological manipulations on the reconsolidation and extinction that could be used to interfere with drug reward memories. Pharmacological agents such as β-adrenergic receptor antagonist propranolol can interfere with reconsolidation to disrupt drug reward memory. Pharmacological agents such as the NMDA receptor glycine site agonists d-cycloserine and d-serine can facilitate extinction and then attenuate the expression of drug reward memory. Besides pharmacological interventions, drug-free behavioral approaches by utilizing the reconsolidation and extinction, such as 'post-retrieval extinction' and 'UCS-retrieval extinction', are also effective to erase or inhibit the recall of drug reward memory. Taken together, pharmacological modulation and non-pharmacological modulation of reconsolidation and extinction are promising approaches to regulate drug reward memory and prevent relapse.

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“…The amount of time spent in each chamber was also recorded for calculation of place preference in this phase (Khaleghzadeh-Ahangar & Haghparast, 2015). …”

Section: Methodsmentioning

confidence: 99%

Reduction of the Morphine Maintenance by Blockade of the NMDA Receptors during Extinction Period in Conditioned Place Preference Paradigm of Rats

Siahposht-Khachaki¹,

Fatahi²,

Haghparast³

2016

BCN

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Introduction:Activation of N-methyl-d-aspartate (NMDA) glutamate receptors in the nucleus accumbens is a component of drug-induced reward mechanism. In addition, NMDA receptors play a major role in brain reward system and activation of these receptors can change firing pattern of dopamine neurons. Blockade of glutamatergic neurotransmission reduces the expression of conditioned place preference (CPP) induced by morphine. Therefore, in this study, by using an NMDA receptor antagonist, DL-2-Amino-5-phosphonopentanoic acid sodium salt (AP5), the role of NMDA receptors on the maintenance and reinstatement of morphine-CPP was investigated.Methods:Forty-three adult male albino Wistar rats were used in this study. After subcutaneous administration of effective dose of morphine (5 mg/kg) during CPP paradigm, the animals received intracerebroventricular doses of AP5(1, 5, and 25 mM/5μL saline) during extinction period (free morphine stage). Conditioning score was recorded during extinction period and reinstatement phase. Besides, another group of the animals received a single dose administration of AP5(5 mM) just before the administration of ineffective dose of morphine (1 mg/kg) in reinstatement phase.Results:The results revealed that two doses of this antagonist (5 and 25 mM) significantly shortened the extinction period of morphine-CPP but did not reduce reinstatement induced by priming dose of morphine. Moreover, the single dose administration of AP5(5 mM) just before prime-morphine injection decreased reinstatement of morphine-CPP.Conclusion:These findings indicate that blockade of NMDA receptors during extinction period reduces maintenance but not reinstatement of morphine. In addition, blocking these receptors in reinstatement phase decreases reinstatement to extinguished morphine.

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Intra-accumbal CB1 receptor blockade reduced extinction and reinstatement of morphine

Cited by 31 publications

References 37 publications

The Opioid-Addicted Tetrapartite Synapse

The Opioid-Addicted Tetrapartite Synapse

Modulating reconsolidation and extinction to regulate drug reward memory

Reduction of the Morphine Maintenance by Blockade of the NMDA Receptors during Extinction Period in Conditioned Place Preference Paradigm of Rats

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