Extinction of appetitive learning is disrupted by cycloheximide and propranolol in the sand maze in rats

Cohen, Joshua L.; Gotthard, Gretchen Hanson

doi:10.1016/j.nlm.2011.02.011

Cited by 11 publications

(8 citation statements)

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“…: 46–49]. Note that amnestic cycloheximide doses are much lower in rats (1–3 mg/kg: [26,50,51]) than in mice, consistent with a similar difference in LD50s for rats and mice. Cycloheximide doses of 120–150 mg/kg result in approximately 95% inhibition of brain protein synthesis as measured 30–60 min after injection [21,52–54]; the dose of 30 mg/kg produces approximately 80% inhibition of brain protein synthesis [21].…”

Section: Methodssupporting

confidence: 58%

Cycloheximide impairs and enhances memory depending on dose and footshock intensity

Gold

Wrenn

2012

Behavioural Brain Research

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This experiment examined the effects on memory of interactions of cycloheximide dose and training foot shock intensity. Mice received injections of cycloheximide (120 mg/kg, s.c.) or saline 30 min prior to inhibitory avoidance training with shock intensities of 100, 150, 250 or 300 µA (1 sec duration). Memory was tested 48 hr later. The saline control mice showed increasing memory latencies as a function of shock intensity. The ability of cycloheximide to impair memory increased as the training shock intensity increased. In a second experiment, mice were trained with a 200 µA (1 sec duration) shock and received injections of saline or cycloheximide at one of several doses (30, 60 or 120 mg/kg). Under these training conditions, cycloheximide enhanced memory in an inverted-U dose-response manner. These findings are consistent with prior findings suggesting that protein synthesis inhibitors act on memory by altering modulators of memory formation as a secondary consequence of the inhibition of protein synthesis rather than by interfering with training-initiated synthesis of proteins required for memory formation.

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Section: Methodssupporting

confidence: 58%

Cycloheximide impairs and enhances memory depending on dose and footshock intensity

Gold

Wrenn

2012

Behavioural Brain Research

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“…PROP may have facilitated extinction learning instead of disrupting reconsolidation. However, since extinguished memories can be reinstated after retraining [30], and PROP seems to impair rather than facilitate extinction [31], [32], this explanation is rather unlikely. Somewhat consistent with our results, post-retrieval PROP treatment has previously been shown to disrupt the reconsolidation and reinstatement of cocaine-induced CPP, albeit that a single PROP treatment interfered with reconsolidation, but that repeated post-retrieval PROP treatments were necessary for blockade of reinstatement [22].…”

Section: Discussionmentioning

confidence: 99%

β-Adrenoreceptor Stimulation Mediates Reconsolidation of Social Reward-Related Memories

2012

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BackgroundIn recent years, the notion that consolidated memories become transiently unstable after retrieval and require reconsolidation to persist for later use has received strong experimental support. To date, the majority of studies on reconsolidation have focused on memories of negative emotions, while the dynamics of positive memories have been less well studied. Social play, the most characteristic social behavior displayed by young mammals, is important for social and cognitive development. It has strong rewarding properties, illustrated by the fact that it can induce conditioned place preference (CPP). In order to understand the dynamics of positive social memories, we evaluated the effect of propranolol, a β-adrenoreceptor antagonist known to influence a variety of memory processes, on acquisition, consolidation, retrieval and reconsolidation of social play-induced CPP in adolescent rats.Methodology/Principal FindingsSystemic treatment with propranolol, immediately before or after a CPP test (i.e. retrieval session), attenuated CPP 24 h later. Following extinction, CPP could be reinstated in saline- but not in propranolol-treated rats, indicating that propranolol treatment had persistently disrupted the CPP memory trace. Propranolol did not affect social play-induced CPP in the absence of memory retrieval or when administered 1 h or 6 h after retrieval. Furthermore, propranolol did not affect acquisition, consolidation or retrieval of social play-induced CPP.Conclusions/SignificanceWe conclude that β-adrenergic neurotransmission selectively mediates the reconsolidation, but not other processes involved in the storage and stability of social reward-related memories in adolescent rats. These data support the notion that consolidation and reconsolidation of social reward-related memories in adolescent rats rely on distinct neural mechanisms.

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“…Additionally, propranolol has been shown to impair consolidation of declarative memory in humans (McGaugh 2000) and to block bicuculline-induced enhancement of extinction consolidation in animals (Berlau and McGaugh 2006). In the case of extinction learning, a number of recent infrahuman studies suggest that propranolol retards extinction of both fear-based context conditioning (Do-Monte et al 2010) and appetitive sand maze learning (Cohen and Gotthard 2011). The former of these two studies is of special relevance insofar as it indicates that a single administration of propranolol does not affect the rate of extinction, a finding that is in agreement with three previous studies (Cain et al 2004; Rodriguez-Romaguera et al 2009; Terry et al 1990).…”

Section: Discussionmentioning

confidence: 99%

A double blind, placebo-controlled study of the effects of post-retrieval propranolol on reconsolidation of memory for craving and cue reactivity in cocaine dependent humans

et al. 2013

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Rationale/Objectives This study examined the effects of propranolol vs. placebo, administered immediately after a 'retrieval' session of cocaine cue exposure (CCE), on craving and physiological responses occurring 24 hr. later during a subsequent 'test' session of CCE. It was hypothesized that compared to placebo-treated cocaine-dependent (CD) individuals, propranolol-treated CD individuals would evidence attenuated craving and physiological reactivity during the test session. Secondarily, it was expected that group differences identified in the test session would be evident at a 1-week follow-up CCE session. Exploratory analyses of treatment effects on cocaine use were also performed at follow-up. Methods CD participants received either 40 mg propranolol or placebo immediately following a 'retrieval' CCE session. The next day, participants received a 'test' session of CCE that was identical to the 'retrieval' session except no medication was administered. Participants underwent a ‘follow-up’ CCE session 1-week later. Craving and other reactivity measures were obtained at multiple time points during the CCE sessions. Results Propranolol- vs. placebo-treated participants evidenced significantly greater attenuation of craving and cardiovascular reactivity during the test session. Analysis of the follow-up CCE session data did not reveal any group differences. Although there was no evidence of treatment effects on cocaine use during follow-up, this study was insufficiently powered to rigorously evaluate differential cocaine use. Conclusions This double-blind, placebo-controlled laboratory study provides the first evidence that propranolol administration following CCE may modulate memories for learning processes that subserve cocaine craving/cue reactivity in CD humans. Alternative interpretations of the findings were considered and implications of the results for treatment were noted.

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Extinction of appetitive learning is disrupted by cycloheximide and propranolol in the sand maze in rats

Cited by 11 publications

References 60 publications

Cycloheximide impairs and enhances memory depending on dose and footshock intensity

Cycloheximide impairs and enhances memory depending on dose and footshock intensity

β-Adrenoreceptor Stimulation Mediates Reconsolidation of Social Reward-Related Memories

A double blind, placebo-controlled study of the effects of post-retrieval propranolol on reconsolidation of memory for craving and cue reactivity in cocaine dependent humans

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