Single dose propranolol does not affect physiologic or emotional reactivity to smoking cues

Abstract

Background Smoking cue exposure reactivates salient smoking-related memories, triggering craving to smoke, a phenomenon associated with maintenance of smoking behavior and relapse after periods of abstinence. Acute β-adrenergic blockade with propranolol reduces physiologic reactivity during subsequent recollection of traumatic events by inhibiting reconsolidation of reactivated memories in a process called memory reconsolidation blockade. Objective To determine whether a single dose of propranolol prior to retrieval of smoking-related memories reduces subsequent physiologic reactivity to personally salient smoking imagery scripts in current smokers. Methods Fifty-four overnight-abstinent, adult smokers received single dose propranolol or placebo prior to reactivation of smoking-related memories in a randomized, double-blind, placebo-controlled trial and resumed smoking afterward. One week later, skin conductance (SC), heart rate (HR) left corrugator electromyogram (EMG), self-reported emotional state and craving were assessed following script driven imagery with neutral and personalized smoking-related scripts. Results Smoking scripts were associated with increased physiologic activation (SC, HR, EMG), craving and negative emotional state compared with neutral scripts. Propranolol did not moderate the effect of script type on any outcome. Conclusion Personalized smoking script-driven imagery robustly increased physiologic activation, negative emotional state and craving, and a single dose of propranolol prior to memory reactivation did not moderate this effect.

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

“…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).…”

Selective Inhibition of Amygdala Neuronal Ensembles Encoding Nicotine-Associated Memories Inhibits Nicotine Preference and Relapse

“…However, as mentioned in the introductory paragraphs, with few exceptions (15,16), the translation of these preclinical studies to human addicts has not been successful (19–21). This state of affairs, and the realization that a major limitation of CS-induced retrieval and reconsolidation procedures is that the neuropharmacological manipulations interfere only with reconsolidation of memories selectively associated with the reactivated CS without affecting memories associated with other CSs or the UCS itself (25–27), inspired us to develop alternative memory reconsolidation interference procedures where the drug reward memory is reactivated by exposure to the drug itself (the UCS).…”

“…However, with few exceptions (15,16), the translation of these preclinical studies has not been successful. For example, the β-adrenoceptor blocker propranolol, which interferes with CS-induced retrieval and reconsolidation of drug reward memories in animal models (13,14,17,18), was ineffective in translational studies with human drug users (19–21). …”

Metabotropic glutamate receptor 5 as a potential target for smoking cessation

“…Interestingly, memory reactivation makes specific drug memory vulnerable to selective and safe blockade by drug treatment (Milton and Everitt 2010). The potential application of such as strategy has also been proposed for smoking cessation and tested for inhibition by pharmacological intervention in humans (Pachas et al 2015) and with post-reactivation extinction in animals with conflicting findings.…”