***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Posttraumatic stress disorder ( PTSD ) may involve over-consoli date d emotional memories of the traumatic event . Reactivation ( RP ) can return a memory to an unstable state , from which it must be restabilized ( reconsoli date d ) if it is to persist . Pharmacological agents administered while the memory is unstable have been shown to impair reconsolidation . The N-methyl-d-aspartate ( NMDA ) partial agonist d-cycloserine ( DCS ) may promote memory destabilization . In the three studies reported here , we investigated whether the β-adrenergic blocker propranolol or the glucocorticoid ( GR ) antagonist mifepristone , given at the time of traumatic memory reactivation , could reduce PTSD symptoms and physiological responding during subsequent traumatic imagery . Individuals with PTSD were r and omized as follows : Study One :  propranolol with memory reactivation ( n=10 ) or without reactivation ( n=8 ) ; Study Two :  reactivation mifepristone ( n=13 ) , non-reactivation ( NRP ) mifepristone ( n=15 ) , or double placebo ( PL ) ( n=15 ) ; Study Three  : reactivation mifepristone plus d-cycloserine ( n=16 ) , or two placebos ( n=15 ) . Subjects underwent memory retrieval by describing their traumatic event . A week later they engaged in script-driven traumatic mental imagery , while heart rate ( HR ) , skin conductance ( SC ) , and facial electromyogram ( EMG ) responses were measured . There were no significant group differences in physiological responsivity or change in PTSD symptoms in any of the studies . These results do not support successful blockade of reconsolidation of traumatic memories in PTSD When a memory is recalled , it may again exist in a labile state and stored information becomes amenable to change , a psychobiological process known as reconsolidation . Exposure therapy for anxiety disorders involves accessing a fear memory and modifying it with less fearful information . A pre clinical study reported that providing a reminder of a fear memory 10 min prior to extinction training in humans decreased fear up to 1 year later ( Schiller et al. , 2010 ) . Methods : For this pilot clinical study , we used virtual reality exposure therapy ( VRE ) for fear of flying ( FoF ) to determine if using a cue to reactivate the memory of the feared stimulus 10 min prior to exposure sessions leads to fewer anxiety‐related behaviors and a more durable response compared to a neutral cue . FoF participants ( N = 89 ) received four sessions of anxiety management training followed by four sessions of VRE . Participants were r and omly assigned to receive an FoF cue ( reactivation group ) or a neutral cue ( control group ) prior to the VRE sessions . Heart rate ( HR ) and skin conductance levels ( SCLs ) were collected during posttreatment and 3‐month follow‐up assessment s as objective markers of fear responding . Results : Treatment was effective and all clinical measures improved equally between groups at posttreatment with maintained gains through follow‐ups . Significant differences were identified with regard to HR and SCL indices . Conclusions : These results suggest that memory reactivation prior to exposure therapy did not have an impact on clinical measures but may enhance the effect of exposure therapy at the physiological level Sixteen alcohol abusers who had completed detoxification were presented with seven different types of alcohol and non-alcohol related stimuli . The sight and smell of the alcoholic beverage most commonly consumed by each subject elicited the largest change in response for measures of heart rate , desire to drink , and self-reported withdrawal symptoms . Beverages progressively more different from the preferred one produced responses of consistently lower magnitude . In the second phase of the study , 10 subjects were exposed to 20 presentations of the sight and smell of their preferred drink . A gradual reduction in the magnitude of the response for all three measures was observed over the 20 presentations . These results were discussed in terms of a conditioning interpretation of cue reactivity . They indicate the need for cue exposure programs to be based on the particular drinking history of the individual Rationale Pre clinical reconsolidation research offers the first realistic opportunity to pharmacologically weaken the maladaptive memory structures that support relapse in drug addicts .  N-methyl D-aspartate receptor ( NMDAR ) antagonism is a highly effective means of blocking drug memory reconsolidation . However , no research using this approach exists in human addicts . Objectives The objective of this study was to assess the potential and clinical outcomes of blocking the reconsolidation of cue-smoking memories with memantine in quitting smokers . Methods Fifty-nine dependent and motivated to quit smokers were r and omised to one of three groups receiving the following : ( 1 ) memantine with or ( 2 ) without reactivation of associative cue-smoking memories or ( 3 ) reactivation with placebo on their target quit day in a double-blind manner . Participants aim ed to abstain from smoking for as long as possible . Levels of smoking and FTND score were assessed prior to intervention and up to a year later . Primary outcome was latency to relapse . Subjective craving measures and attentional bias to smoking cues were assessed in-lab . Results All study groups successfully reduced their smoking up to 3 months . Memantine in combination with smoking memory reactivation did not affect any measure of smoking outcome , reactivity or attention capture to smoking cues . Conclusions Brief exposure to smoking cues with memantine did not appear to weaken these memory traces . These findings could be due to insufficient reconsolidation blockade by memantine or failure of exposure to smoking stimuli to destabilise smoking memories . Research assessing the treatment potential of reconsolidation blockade in human addicts should focus on identification of tolerable drugs that reliably block reward memory reconsolidation and retrieval procedures that reliably destabilise strongly trained memories 1 . Hazelrigg , T. Cell 95 , 451–460 ( 1998 ) . 2 . Tiedge , H. , Bloom , F. E. & Richter , D. Science 283 , 186–187 ( 1999 ) . 3 . Huang , E. P. Curr . Biol . 9 , R168–R170 ( 1999 ) . 4 . Gao , F. B. Bioessays 20 , 7–78 ( 1998 ) . 5 . Kuhl , D. & Skehel , P. Curr . Opin . Neurobiol . 8 , 600–606 ( 1998 ) . 6 . Palade , G. Science 189 , 347–358 ( 1975 ) . 7 . Spacek , J. & Harris , K. M. J. Neurosci 17 , 190–203 ( 1997 ) . 8 . Berridge , M. J. Neuron 21 , 13–26 ( 1998 ) . 9 . Matlack , K. E. S. , Mothes , W. & Rapoport , T. A. Cell 92 , 381–390 ( 1998 ) . 10 . Gorlich , D. & Rapoport , T. A. Cell 75 , 615–630 ( 1993 ) . 11 . Bailey , C. H. , Bartsch , D. & K and el , E. R. Proc . Natl . Acad . Sci . USA 93 , 13445–13452 ( 1996 ) . 12 . Schuman , E. M. Neuron 18 , 339–342 ( 1997 ) . 13 . Pelham , H. R. Trends . Biochem . Sci . 15 , 483–486 ( 1990 ) . 14 . Lledo , P.M. , Zhang , X. , Sudhof , T. C. , Malenka , R. C. & Nicoll , R. A. Science 279 , 399–403 ( 1998 ) . 15 . Chan , J. , Aoki , C. & Pickel , V. M. J. Neurosci . Methods 33 , 113–127 ( 1990 ) . brief communications 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 re collection of traumatic events by inhibiting reconsolidation of reactivated memories in a process called memory reconsolidation blockade . Objective The objective of this study is 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 a single-dose propranolol or placebo prior to reactivation of smoking-related memories in a r and omized , 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 BACKGROUND Reactivated memories go through a process of reconsolidation , during which they are malleable and susceptible to modification . Strategies targeting the interruption of memory reconsolidation hold the promise of weakening fear memories that underlie traumatic stress disorders . Although many studies have examined the efficacy of reconsolidation interference strategies with fear memories developed in a laboratory , very few have examined this with trauma-related episodic memories . This study aims to examine whether new learning can interfere with the reconsolidation of trauma-related episodic memories , when the affective content of the new learning and memory match . METHODS Boston-area young adults ( n = 94 ) wrote about negative autobiographical memories ; specifically , their personal memories of the Boston Marathon bombings . Following reactivation , participants were r and omized to receive interference with a negative , positive , neutral , or no story . One week later , participants were tested for memory recall . RESULTS Comparisons between conditions with relevant covariates revealed a significant interfering effect for a negative story , relative to no story , on recall ( P < .05 , 95 % CI [ -3.90 , -0.04 ] ) , d = 0.62 ) . In contrast , the neutral and positive story , relative to no story , result ed in smaller and nonsignificant effects . CONCLUSIONS These findings indicate that reconsolidation interference effects can be achieved for trauma-related episodic memories and the emotional valence of interference material may be an important context ual factor in achieving these effects . This study provides support for further research translating memory reconsolidation findings into treatments for traumatic stress disorders Objectives : Relapse to drug misuse may follow exposure to drug cues that elicit craving . The learned associations , or “ emotional memories , ” that underlie responses to cues may be attenuated or erased by the & bgr;-adrenergic antagonist propranolol during a “ reconsolidation window ” shortly after the memories are reactivated by cues . Methods : We evaluated the effects of propranolol on cue-induced drug cravings in healthy opioid-dependent individuals who used cocaine while receiving methadone maintenance ( n = 33 ) . Participants were asked to recall specific cocaine use and neutral events in an interview ; these events were used to develop personalized auditory script/cue sets . Approximately 1 week later , propranolol ( 40 mg ) or placebo ( r and om assignment , double blind ) was administered orally before presentation of the script/cue sets ; the presentation of the script/cue sets were tested 1 week and 5 weeks after the propranolol/placebo session . Ongoing drug use was monitored via urine screens and self-report in twice-weekly visits . Results : Cue reactivity , as assessed by craving scales and physiological responses , was unexpectedly greater in the propranolol group than in the placebo group . This counterhypothesized group difference was present acutely during propranolol administration and seemed to persist ( without reaching statistical significance ) during the subsequent test sessions . Conclusions : Our results do not support the use of propranolol for cue-induced cocaine craving in opioid-maintained patients OBJECTIVE The authors assessed the efficacy of trauma memory reactivation performed under the influence of propranolol , a noradrenergic beta-receptor blocker , as a putative reconsolidation blocker , in reducing symptoms of  posttraumatic stress disorder ( PTSD ) . METHOD This was a 6-week , double-blind , placebo-controlled , r and omized clinical trial in 60 adults diagnosed with long-st and ing PTSD .  Propranolol or placebo was administered 90 minutes before a brief memory reactivation session , once a week for 6 consecutive weeks . The hypothesis predicted a significant treatment effect of trauma reactivation with propranolol compared with trauma reactivation with placebo in reducing P 
    Output:
    
Conclusion Modification of naturalistic maladaptive memories during reconsolidation appears to be a viable treatment strategy for substance use and phobias/trauma disorders .