Repeated alcohol extinction sessions in conjunction with MK-801, but not yohimbine or propranolol, reduces subsequent alcohol cue-induced responding in rats

Williams, Keith; Harding, Kaitlyn M.

doi:10.1016/j.pbb.2013.11.020

Cited by 8 publications

(8 citation statements)

References 48 publications

(56 reference statements)

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“…In contrast to the original hypothesis, post-reactivation propranolol had no effect on cue-induced reinstatement, indicative of no effect on It is not surprising, however, that propranolol failed to block reconsolidation as measured by cue-induced reinstatement. Previous research indicates that propranolol is not always effective at interfering with reconsolidation in both rodents Font and Cunningham 2012;Milton et al 2012;Williams and Harding 2014) and humans (Tollenaar et al 2009;Bos et al 2014;Pachas et al 2015;Spring et al 2015;Wood et al 2015), and replications of experiments even within the same laboratory have produced differing results (Kindt et al 2009;Bos et al 2014). Some explanations for these inconsistencies include the ability of propranolol to preferentially affect emotional memories over neutral memories (Schwabe et al 2012a,b), individual differences in participants (Soeter and Kindt 2013), and the mnemonic paradigm under investigation Wei and Li 2014).…”

Section: Discussionmentioning

confidence: 99%

“…While post-reactivation propranolol has been shown to reduce conditioned reinforcement in a rodent model of cocaine self-administration (Milton et al 2008), preliminary data from the same laboratory indicate that under the same conditions post-reactivation propranolol may not block cue-induced reinstatement Everitt 2009, 2010), which is supported by the present results. Furthermore, while alcohol conditioned reinforcement is blocked by post-reactivation propranolol similarly to cocaine (Milton et al 2008;Schramm et al 2015), alcohol conditioned motivation and approach are not Milton et al 2012), and the effect of propranolol on cue-induced reinstatement to alcohol-seeking is unclear (Wouda et al 2010;Williams and Harding 2014). Thus, it is likely that propranolol selectively or preferentially modifies the reconsolidation of conditioned reinforcement.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Inhibition of protein synthesis but not β-adrenergic receptors blocks reconsolidation of a cocaine-associated cue memory

Dunbar

Taylor

2016

Learn. Mem.

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Previously consolidated memories have the potential to enter a state of lability upon memory recall, during which time the memory can be altered before undergoing an additional consolidation-like process and being stored again as a longterm memory. Blocking reconsolidation of aberrant memories has been proposed as a potential treatment for psychiatric disorders including addiction. Here we investigated of the effect of systemically administering the protein synthesis inhibitor cycloheximide or the b-adrenergic antagonist propranolol on reconsolidation. Rats were trained to self-administer cocaine, during which each lever press resulted in the presentation of a cue paired with an intravenous infusion of cocaine. After undergoing lever press extinction to reduce operant responding, the cue memory was reactivated and rats were administered systemic injections of propranolol, cycloheximide, or vehicle. Post-reactivation cycloheximide, but not propranolol, resulted in a reactivation-dependent decrease in cue-induced reinstatement, indicative of reconsolidation blockade by protein synthesis inhibition. The present data indicate that systemically targeting protein synthesis as opposed to the b-adrenergic system may more effectively attenuate the reconsolidation of a drug-related memory and decrease drug-seeking behavior.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Inhibition of protein synthesis but not β-adrenergic receptors blocks reconsolidation of a cocaine-associated cue memory

Dunbar

Taylor

2016

Learn. Mem.

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“…In this model, rodents are trained to lever press or nose poke for rewards, such as food, intravenous drug infusion, or intracranial stimulation (eg, of the lateral hypothalamus). Experiments have revealed that systemic propranolol injections administered after memory retrieval disrupt context-or cue-driven sucrose seeking (Diergaarde et al, 2006;Milton et al, 2008b), cocaine seeking (Milton et al, 2008b), and ethanol seeking (Wouda et al, 2010) within the SA paradigm (but see Milton and Everitt, 2010;Williams and Harding, 2014). However, these convincing experiments have been overshadowed by studies revealing no effect of propranolol when administered before memory retrieval (Lee and Everitt, 2008;Milton and Everitt, 2010).…”

Section: Rodent Sa Studiesmentioning

confidence: 99%

“…Synaptic plasticity is a critical mechanism for reconsolidation (Clem and Huganir, 2010). Moreover, NMDA receptor Impaired Sucrose (CR) Milton et al (2008b) Impaired Cocaine (CR) Milton et al (2008b) No effect Cocaine (reinstatement) Milton and Everitt (2010) Impaired EtOH (extinction) Wouda et al (2010) No effect EtOH (extinction) Williams and Harding (2014) Before No effect Sucrose (PCA) Lee and Everitt (2008) No effect Sucrose (PIT) Lee and Everitt (2008) No effect EtOH (PCA) Milton et al (2012) No effect EtOH (PIT) Milton et al (2012) Abbreviations: CR, conditioned reinforcement; PCA, Pavlovian conditioned approach; PIT, Pavlovian-to-instrumental transfer. Summary of findings for research examining the effectiveness of propranolol for reconsolidation blockade within the SA paradigm.…”

Section: Cellular Mechanismsmentioning

confidence: 99%

Noradrenergic Regulation of Fear and Drug-Associated Memory Reconsolidation

Otis

Werner

Mueller

2014

Neuropsychopharmacol

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Emotional and traumatic experiences lead to the development of particularly strong memories that can drive neuropsychiatric disorders, such as posttraumatic stress disorder (PTSD) and drug addiction. Disruption of these memories would therefore serve as a powerful treatment option, and targeting the pathologic emotional, but not declarative, component of a memory would be ideal for clinical intervention. Research reveals that after retrieval of a consolidated memory, the memory can be destabilized, and must then be reconsolidated through synaptic plasticity to allow subsequent retrieval. Disruption of reconsolidation-related plasticity would therefore impair specific, reactivated memories. Noradrenergic signaling strengthens synaptic plasticity and is essential for encoding the emotional components of memory. Consistent with this, investigations have now revealed that noradrenergic signaling is a critical mechanism for reconsolidation of emotional memories in rodent and human models. Here, we discuss these investigations and promising clinical trials indicating that disruption of noradrenergic signaling during reconsolidation may abolish the pathologic emotional, but not declarative, component of memories allowing alleviation of neuropsychiatric disorders including PTSD and drug addiction.

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“…The acquisition of these appetitive conditioned responses depends on the ventral tegmental area, striatum, amygdala, and, for contextual information, the hippocampus (Everitt 2014; Everitt and Robbins 2005; Robbins et al 2008). Memory reactivation combined with noradrenergic antagonists has been reported to reduce self-administration behaviour of cocaine and sucrose but may be more limited for alcohol (Diergaarde et al 2006; Milton et al 2008; Williams and Harding 2014; Wouda et al 2010). In addition, studies have reported an attenuation of CPP by beta-blockers following memory reactivation (Bernardi et al 2006, 2009; Fricks-Gleason and Marshall 2008; Robinson and Franklin 2007), although effects have not always been equally strong in that memory has been found to recover over time (Fricks-Gleason and Marshall 2008; Robinson and Franklin 2007), and more remote memories may be more resistant to modification (Robinson and Franklin 2010; Robinson et al 2011).…”

Section: Biological Interventions Targeting Reconsolidationmentioning

confidence: 99%

Translational Approaches Targeting Reconsolidation

Kroes

Schiller

LeDoux

et al. 2015

Translational Neuropsychopharmacology

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Maladaptive learned responses and memories contribute to psychiatric disorders that constitute a significant socio-economic burden. Primary treatment methods teach patients to inhibit maladaptive responses, but do not get rid of the memory itself, which explains why many patients experience a return of symptoms even after initially successful treatment. This highlights the need to discover more persistent and robust techniques to diminish maladaptive learned behaviours. One potentially promising approach is to alter the original memory, as opposed to inhibiting it, by targeting memory reconsolidation. Recent research shows that reactivating an old memory results in a period of memory flexibility and requires restorage, or reconsolidation, for the memory to persist. This reconsolidation period allows a window for modification of a specific old memory. Renewal of memory flexibility following reactivation holds great clinical potential as it enables targeting reconsolidation and changing of specific learned responses and memories that contribute to maladaptive mental states and behaviours. Here, we will review translational research on non-human animals, healthy human subjects, and clinical populations aimed at altering memories by targeting reconsolidation using biological treatments (electrical stimulation, noradrenergic antagonists) or behavioural interference (reactivation–extinction paradigm). Both approaches have been used successfully to modify aversive and appetitive memories, yet effectiveness in treating clinical populations has been limited. We will discuss that memory flexibility depends on the type of memory tested and the brain regions that underlie specific types of memory. Further, when and how we can most effectively reactivate a memory and induce flexibility is largely unclear. Finally, the development of drugs that can target reconsolidation and are safe for use in humans would optimize cross-species translations. Increasing the understanding of the mechanism and limitations of memory flexibility upon reactivation should help optimize efficacy of treatments for psychiatric patients.

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Repeated alcohol extinction sessions in conjunction with MK-801, but not yohimbine or propranolol, reduces subsequent alcohol cue-induced responding in rats

Cited by 8 publications

References 48 publications

Inhibition of protein synthesis but not β-adrenergic receptors blocks reconsolidation of a cocaine-associated cue memory

Inhibition of protein synthesis but not β-adrenergic receptors blocks reconsolidation of a cocaine-associated cue memory

Noradrenergic Regulation of Fear and Drug-Associated Memory Reconsolidation

Translational Approaches Targeting Reconsolidation

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