Potentiated Reinstatement of Cocaine-Seeking Behavior Following D-amphetamine Infusion into the Basolateral Amygdala

Ledford, Christopher C.; Fuchs, Rita A.; See, Ronald E.

doi:10.1038/sj.npp.1300249

Cited by 42 publications

(31 citation statements)

References 56 publications

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“…For example, cue-induced relapse of cocaine-seeking behavior is associated with increased dopamine release in the BLA and is attenuated by blockade of dopamine but not glutamate receptors in the BLA (See et al, 2001;Di Ciano and Everitt, 2004). These results are further supported by observations that intra-BLA infusions of a nonspecific dopamine agonist potentiate cocaine-seeking behavior (Ledford et al, 2003) and that intra-BLA administration of D 1 dopamine receptor antagonists reverses cue-induced cocaine relapse and the corresponding increase in c-fos expression, a marker for neural activation (Ciccocioppo et al, 2001b). Although limited, there is also evidence suggesting that the integrity of the BLA is necessary for cueinduced reinstatement of heroin-seeking behavior (Fuchs and See, 2002).…”

Section: Discussionsupporting

confidence: 75%

Attenuation of Cue-Induced Heroin-Seeking Behavior by Cannabinoid CB1 Antagonist Infusions into the Nucleus Accumbens Core and Prefrontal Cortex, but Not Basolateral Amygdala

Alvarez-Jaimes

Polis

Parsons

2007

Neuropsychopharmacol

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As with other drugs of abuse, heroin use is characterized by a high incidence of relapse following detoxification that can be triggered by exposure to conditioned stimuli previously associated with drug availability. Recent findings suggest that cannabinoid CB 1 receptors modulate the motivational properties of heroin-conditioned stimuli that induce relapse behavior. However, the neural substrates through which CB 1 receptors modulate cue-induced heroin seeking have not been elucidated. In this study, we evaluated alterations in cue-induced reinstatement of heroin-seeking behavior produced by infusions of the CB 1 receptor antagonist SR 141716A (0, 0.3 and 3 mg per side) delivered into the prefrontal cortex (PFC), nucleus accumbens (NAC), and basolateral amygdala (BLA) of rats. Results show that following extinction of operant behavior the presentation of a discriminative stimulus conditioned to heroin availability reinstated nonreinforced lever pressing to levels comparable to preextinction levels. Intra-PFC SR 141716A dose-dependently reduced cue-induced reinstatement of heroin seeking, with a significant reduction following the 3 mg per side dose. In the NAC, both SR 141716A doses induced a significant reduction in cue-induced reinstatement, with the highest dose completely blocking the effect of the cue. In contrast, intra-BLA SR 141716A did not alter cue-induced reinstatement of responding while systemic administration of this antagonist (3 mg/kg, i.p.) significantly blocked cue-induced reinstatement in all three-placement groups (BLA, PFC, and NAC). These findings provide new insights into the neural mechanisms through which CB 1 receptors modulate the motivational properties of heroin-associated cues inducing relapse.

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Section: Discussionsupporting

confidence: 75%

Attenuation of Cue-Induced Heroin-Seeking Behavior by Cannabinoid CB1 Antagonist Infusions into the Nucleus Accumbens Core and Prefrontal Cortex, but Not Basolateral Amygdala

Alvarez-Jaimes

Polis

Parsons

2007

Neuropsychopharmacol

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“…In addition, reversible inactivation of the BLA by lidocaine can block both the acquisition and expression of the response-maintaining properties of a CS under both second-order and reinstatement conditions [119,145,158]. Recent studies have also shown that direct microinfusion of D-amphetamine into the BLA can potentiate cue-triggered relapse to cocaine seeking in a dose-dependent manner without affecting extinction responding [166]. Furthermore, electrical or chemical stimulation of the BLA can reinstate cocaine-seeking behavior following behavioral extinction of the cocaine-seeking habit [129], as can electrical stimulation of the hippocampus, another brain structure implicated in the storage and retrieval of memories underlying the cue-incentive properties of addictive drugs [294].…”

Section: Discussionmentioning

confidence: 99%

The role of central dopamine D3 receptors in drug addiction: a review of pharmacological evidence

Heidbreder

Gardner

et al. 2005

Brain Research Reviews

305

249

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The cDNA for the dopamine D 3 receptor was isolated and characterized in 1990. Subsequent studies have indicated that D 3 receptors, as well as D 3 receptor mRNA, are primarily localized in limbic regions in mammals. This finding led to the postulate that D 3 receptors may be involved in drug dependence and addiction. However, this hypothesis has been difficult to test due to the lack of compounds with high selectivity for central D 3 receptors. The interpretation of results from studies using mixed D 2 /D 3 agonists and/or antagonists is problematic because these agents have low selectivity for D 3 over D 2 receptors and it is likely that their actions are primarily related to D 2 receptor antagonism and possibly interaction with other neurotransmitter receptors. Currently, with the synthesis and characterization of new highly selective D 3 receptor antagonists such as SB-277011-A this difficulty has been surmounted. The purpose of the present article is to review, for the first time, the effects of various putative D 3 receptor selective compounds in animal models of drug dependence and addiction. The results obtained with highly selective D 3 receptor antagonists such as SB-277011-A, SB-414796, and NGB-2904 indicate that central D 3 receptors may play an important role in drug-induced reward, drug-taking, and cue-, drug-, and stressinduced reinstatement of drug-seeking behavior. Provided these results can be extrapolated to human drug addicts, they suggest that selective DA D 3 receptor antagonists may prove effective as potential pharmacotherapeutic agents to manage drug dependence and addiction.

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“…TTX inactivation of the DH failed to alter the ability of the cocaine priming injection to reinstate responding (Figure 4b). Cocaine-primed reinstatement of responding was not due to the stress of intraperitoneal drug administration since intraperitoneal administration of saline alone or in combination with intracranial administration of saline fails to reinstate responding (Neisewander et al, 2000;Fuchs et al, 2002a;Fuchs and See, 2002;Ledford et al, 2003).…”

Section: Methodsmentioning

confidence: 96%

The Role of the Dorsomedial Prefrontal Cortex, Basolateral Amygdala, and Dorsal Hippocampus in Contextual Reinstatement of Cocaine Seeking in Rats

Fuchs

Evans

Ledford

et al. 2004

Neuropsychopharmacol

Self Cite

488

517

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The present study tested the hypothesis that separate neural substrates mediate cocaine relapse elicited by drug-associated contextual stimuli vs explicit conditioned stimuli (CSs) and cocaine. Specifically, we investigated the involvement of the dorsal hippocampus (DH), basolateral amygdala (BLA), and dorsomedial prefrontal cortex (dmPFC) in contextual reinstatement of cocaine-seeking behavior and the involvement of the DH in explicit CS-and cocaine-induced reinstatement. Rats were trained to self-administer cocaine in a distinct context or in the presence of CSs paired explicitly with cocaine infusions. Responding of context-trained rats was then extinguished in the previously cocaine-paired or an alternate context, whereas responding of explicit CS-trained rats was extinguished in the absence of the CSs. Subsequently, the target brain regions or anatomical control regions were functionally inactivated using tetrodotoxin (0 or 5 ng/ side), and cocaine-seeking behavior (ie, nonreinforced responses) was assessed in the cocaine-paired context, in the alternate context, in the presence of the explicit CSs, or following cocaine priming (10 mg/kg, i.p.). DH inactivation abolished contextual, but failed to alter explicit CS-or cocaine-induced, reinstatement of cocaine-seeking behavior. BLA or dmPFC inactivation also abolished contextual reinstatement. Conversely, inactivation of the control brain regions failed to alter contextual reinstatement. In conclusion, the DH, BLA, and dmPFC play critical roles in contextual reinstatement. Previous findings suggest that the BLA is critical for explicit CS-induced, but not cocaine-primed, reinstatement and the dmPFC is critical for both explicit CS-induced and cocaine-primed reinstatement. Thus, distinct but partially overlapping neural substrates mediate context-induced, explicit CS-induced, and cocaine-primed reinstatement of extinguished cocaine-seeking behavior.

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Potentiated Reinstatement of Cocaine-Seeking Behavior Following D-amphetamine Infusion into the Basolateral Amygdala

Cited by 42 publications

References 56 publications

Attenuation of Cue-Induced Heroin-Seeking Behavior by Cannabinoid CB1 Antagonist Infusions into the Nucleus Accumbens Core and Prefrontal Cortex, but Not Basolateral Amygdala

Attenuation of Cue-Induced Heroin-Seeking Behavior by Cannabinoid CB1 Antagonist Infusions into the Nucleus Accumbens Core and Prefrontal Cortex, but Not Basolateral Amygdala

The role of central dopamine D3 receptors in drug addiction: a review of pharmacological evidence

The Role of the Dorsomedial Prefrontal Cortex, Basolateral Amygdala, and Dorsal Hippocampus in Contextual Reinstatement of Cocaine Seeking in Rats

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