Central but not peripheral beta-adrenergic antagonism blocks reconsolidation for a morphine place preference

Robinson, Michael J.; Franklin, Keith B.J.

doi:10.1016/j.bbr.2007.05.023

Cited by 68 publications

(71 citation statements)

References 40 publications

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“…These results are consistent with previous work demonstrating post-retrieval impairment of a cocaine CPP using the nonspecific b-AR antagonist propranolol (Bernardi et al 2006) and suggest that the effect of propranolol demonstrated in this previous study may be mediated by the b 2 -AR. The results presented here are also consistent with a number of other studies demonstrating impairment of possible reconsolidation processes via systemic b-AR blockade in drug-mediated learning paradigms, including morphine CPP (Robinson and Franklin 2007) and a cocaine cue-mediated acquisition of a new response paradigm (Milton et al 2008), and several other nondrug learning tasks (Roullet and Sara 1998;Przybyslawski et al 1999;Diergaarde et al 2006;Abrari et al 2008). Propranolol administered following retrieval of a fear memory in humans has recently been reported to completely abolish the expression of fear (Kindt et al 2009), and thus our results extend findings in both human and animal studies by suggesting that the disruption of maladaptive memories can be achieved via more targeted AR antagonism.…”

Section: Discussionsupporting

confidence: 90%

“…Although the theoretical mechanisms underlying reconsolidation remain unclear, the behavioral effects have been demonstrated across many different learning paradigms using a variety of pharmacological manipulations (for review, see Tronson and Taylor 2007;Diergaarde et al 2008). Studies with aversive and appetitive preparations, including drug reward-mediated learning, have demonstrated that the noradrenergic system is important for these post-retrieval memory processes (Przybyslawski et al 1999;Debiec and Ledoux 2004;Bernardi et al 2006;Diergaarde et al 2006;Robinson and Franklin 2007;Abrari et al 2008;FricksGleason and Marshall 2008;Milton et al 2008). For example, using an animal model of cocaine-conditioned behaviors, Bernardi et al (2006) demonstrated that systemic post-retrieval administration of propranolol impaired a subsequent conditioned place preference (CPP), suggesting that b-adrenergic receptors (b-ARs) play an important role in processes occurring following drug memory retrieval.…”

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confidence: 99%

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Post-retrieval disruption of a cocaine conditioned place preference by systemic and intrabasolateral amygdala β₂- and α₁-adrenergic antagonists

Bernardi¹,

Ryabinin²,

Berger³

et al. 2009

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Previous work has demonstrated post-retrieval impairment in associative learning paradigms, including those mediated by drugs of abuse, using nonspecific b-adrenergic receptor (b-AR) antagonists. Remarkably little is known about the role of the specific b-AR subtypes, or other adrenergic receptors, in these effects. The current study examined the effects of b 1 and b 2 , as well as a 1 -adrenergic receptor antagonism following retrieval of a cocaine conditioned place preference (CPP). We found that rats administered the b 2 antagonist ICI 118,551 (8 mg/kg intraperitoneal [IP]) or the a 1 antagonist prazosin (1 mg/kg IP) following a drug-free test for CPP showed attenuated preference during a subsequent test, while the b 1 antagonist betaxolol (5 or 10 mg/kg IP) and a lower dose of prazosin (0.3 mg/kg IP) had no effect. Furthermore, posttest microinfusion of ICI 118,551 (6 nmol/side) or prazosin (0.5 nmol/side) into the basolateral amygdala (BLA) also impaired a subsequent preference. Systemic or intra-BLA ICI 118,551 or prazosin administered to rats in their home cages, in the absence of a preference test, had no effect on CPP 24 h later. ICI 118,551 also attenuated the FOS response in the BLA induced by the CPP test. These results are the first to demonstrate a role for a 1 -and b 2 -specific adrenergic mechanisms in post-retrieval memory processes. These systemic and site-specific injections, as well as the FOS immunohistochemical analyses, implicate the importance of specific noradrenergic signaling mechanisms within the BLA in post-retrieval plasticity.

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Section: Discussionsupporting

confidence: 90%

mentioning

confidence: 99%

Post-retrieval disruption of a cocaine conditioned place preference by systemic and intrabasolateral amygdala β₂- and α₁-adrenergic antagonists

Bernardi¹,

Ryabinin²,

Berger³

et al. 2009

Learn. Mem.

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show abstract

“…Recent investigations have demonstrated a role for b-adrenergic signaling in the reconsolidation of drugassociated memories. Post-retrieval propranolol treatment disrupts subsequent expression of both cocaine-and morphine-associated CPP memories (Bernardi et al, 2006;Fricks-Gleason and Marshall, 2008;Robinson and Franklin, 2007), an effect attributable to reconsolidation blockade rather than facilitated extinction learning (Fricks-Gleason and Marshall, 2008). In the present study, we found that pre-retrieval propranolol treatment blocked the initial retrieval of a CPP memory.…”

Section: Time In Chamber (Sec)supporting

confidence: 53%

Inhibition of β-Adrenergic Receptors Induces a Persistent Deficit in Retrieval of a Cocaine-Associated Memory Providing Protection against Reinstatement

Otis

Mueller

2011

Neuropsychopharmacol

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Drug-seeking behavior is maintained by encounters with drug-associated cues. Preventing retrieval of drug-associated memories that these cues provoke would therefore limit relapse susceptibility; however, little is known regarding the mechanisms of retrieval. Here, we show that b-adrenergic receptor activation is necessary for the retrieval of a cocaine-associated memory. Using a conditioned place preference (CPP) procedure, rats were conditioned to associate one chamber, but not another, with cocaine. When administered before a CPP trial, propranolol, but not saline, prevented retrieval of a cocaine-associated CPP. In subsequent drug-free trials, rats previously treated with propranolol continued to show a retrieval deficit, as no CPP was evident. This retrieval deficit was long lasting and robust, as the CPP did not re-emerge during a test for spontaneous recovery 14 days later or reinstate following a priming injection of cocaine. Moreover, the peripheral b-adrenergic receptor antagonist sotalol did not affect retrieval. Thus, retrieval of cocaine-associated memories is mediated by norepinephrine acting at central b-adrenergic receptors. Our findings support the use of propranolol, a commonly prescribed b-blocker, as an adjunct to exposure therapy for the treatment of addiction by preventing retrieval of drugassociated memories during and long after treatment, and by providing protection against relapse.

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“…In human and clinical studies, administration of propranolol before memory reactivation suppresses the behavioral expression of the fear memory (39), and postreactivation treatment reduces symptoms of posttraumatic stress disorder (40,41). In animal studies, propranolol has been shown to inhibit reconsolidation of cocaine-and morphine-conditioned place preference (27,42). Postreactivation propranolol administration also attenuates reconsolidation of memories for craving and cue reactivity in cocaine addicts and abstinent heroin addicts (31,43).…”

Section: Discussionmentioning

confidence: 99%

β-Arrestin–biased signaling mediates memory reconsolidation

Liu

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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A long-standing hypothesis posits that a G protein-coupled signaling pathway mediates β-adrenergic nervous system functions, including learning and memory. Here we report that memory retrieval (reactivation) induces the activation of β1-adrenergic β-arrestin signaling in the brain, which stimulates ERK signaling and protein synthesis, leading to postreactivation memory restabilization. β-Arrestin2-deficient mice exhibit impaired memory reconsolidation in object recognition, Morris water maze, and cocaine-conditioned place preference paradigms. Postreactivation blockade of both brain β-adrenergic Gs protein- and β-arrestin–dependent pathways disrupts memory reconsolidation. Unexpectedly, selective blockade of the Gs/cAMP/PKA signaling but not the β-arrestin/ERK signaling by the biased β-adrenergic ligands does not inhibit reconsolidation. Moreover, the expression of β-arrestin2 in the entorhinal cortex of β-arrestin 2–deficient mice rescues β1-adrenergic ERK signaling and reconsolidation in a G protein pathway-independent manner. We demonstrate that β-arrestin–biased signaling regulates memory reconsolidation and reveal the potential for β-arrestin–biased ligands in the treatment of memory-related disorders.

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Central but not peripheral beta-adrenergic antagonism blocks reconsolidation for a morphine place preference

Cited by 68 publications

References 40 publications

Post-retrieval disruption of a cocaine conditioned place preference by systemic and intrabasolateral amygdala β₂- and α₁-adrenergic antagonists

Post-retrieval disruption of a cocaine conditioned place preference by systemic and intrabasolateral amygdala β₂- and α₁-adrenergic antagonists

Inhibition of β-Adrenergic Receptors Induces a Persistent Deficit in Retrieval of a Cocaine-Associated Memory Providing Protection against Reinstatement

β-Arrestin–biased signaling mediates memory reconsolidation

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Central but not peripheral beta-adrenergic antagonism blocks reconsolidation for a morphine place preference

Cited by 68 publications

References 40 publications

Post-retrieval disruption of a cocaine conditioned place preference by systemic and intrabasolateral amygdala β2- and α1-adrenergic antagonists

Post-retrieval disruption of a cocaine conditioned place preference by systemic and intrabasolateral amygdala β2- and α1-adrenergic antagonists

Inhibition of β-Adrenergic Receptors Induces a Persistent Deficit in Retrieval of a Cocaine-Associated Memory Providing Protection against Reinstatement

β-Arrestin–biased signaling mediates memory reconsolidation

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Post-retrieval disruption of a cocaine conditioned place preference by systemic and intrabasolateral amygdala β₂- and α₁-adrenergic antagonists

Post-retrieval disruption of a cocaine conditioned place preference by systemic and intrabasolateral amygdala β₂- and α₁-adrenergic antagonists