The Efficacy of Lidocaine in Disrupting Cocaine Cue-Induced Memory Reconsolidation

•Lidocaine, a sodium channel blocker, inhibits NMDA receptor activation and suppresses nitric oxide and ERK production, which are crucial for memory reconsolidation.•Treatment-seeking cocaine-dependent participants were randomly assigned in a double-blind design to either receive intravenous lidocai...

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Published inDrug and alcohol dependence Vol. 212; p. 108062
Main Authors Becker, Josh E., Price, Julianne L., Leonard, David, Suris, Alina, Kandil, Enas, Shaw, Meredith, Kroener, Sven, Brown, E Sherwood, Adinoff, Bryon
Format Journal Article
LanguageEnglish
Published Ireland Elsevier B.V 01.07.2020
Elsevier Science Ltd
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ISSN0376-8716
1879-0046
1879-0046
DOI10.1016/j.drugalcdep.2020.108062

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Abstract •Lidocaine, a sodium channel blocker, inhibits NMDA receptor activation and suppresses nitric oxide and ERK production, which are crucial for memory reconsolidation.•Treatment-seeking cocaine-dependent participants were randomly assigned in a double-blind design to either receive intravenous lidocaine immediately following a cocaine craving script (lidocaine/craving), saline following a craving script (saline/craving), or lidocaine following a relaxation script (lidocaine/relax).•One week following the infusion, cue-induced craving was assessed in the same paradigm without an infusion.•Lidocaine administered following craving induction did not decrease subsequent cue-induced craving or cocaine use.•Blocking the reconsolidation of craving-related memories with pharmacological agents remains an important area of investigation. Cue-induced craving memories, linked to drug-seeking behaviors, require key molecular processes for memory reconsolidation. Lidocaine, a sodium channel blocker, inhibits NMDA receptor activation and suppresses nitric oxide and ERK production. These processes are required for memory re-consolidation; inhibiting them may reduce cue-related craving memories in cocaine dependent subjects. To assess the efficacy of lidocaine in decreasing cue-induced cocaine craving and cocaine use. Treatment-seeking cocaine-dependent participants (n = 33, 25 men) were recruited. Personalized craving and relaxation scripts were developed. Participants were then randomly assigned in a double-blind design to either receive intravenous lidocaine immediately following a cocaine craving script (lidocaine/craving), saline following a craving script (saline/craving), or lidocaine following a relaxation script (lidocaine/relax). One week following the infusion, cue-induced craving was assessed in the same paradigm without an infusion. Cocaine use and craving were assessed for 4 weeks following infusion. The administration of lidocaine during craving induction (lidocaine/craving) did not decrease cue-induced craving during craving reactivation one week later or craving and cocaine use over the 4-week follow-up period compared to the saline/craving group. There were no significant differences in craving and cocaine use between the lidocaine/relax and saline/craving groups. Lidocaine administered following craving induction did not decrease subsequent cue-induced craving or cocaine use. Blocking the reconsolidation of craving-related memories with pharmacological agents remains an important area of investigation.
AbstractList •Lidocaine, a sodium channel blocker, inhibits NMDA receptor activation and suppresses nitric oxide and ERK production, which are crucial for memory reconsolidation.•Treatment-seeking cocaine-dependent participants were randomly assigned in a double-blind design to either receive intravenous lidocaine immediately following a cocaine craving script (lidocaine/craving), saline following a craving script (saline/craving), or lidocaine following a relaxation script (lidocaine/relax).•One week following the infusion, cue-induced craving was assessed in the same paradigm without an infusion.•Lidocaine administered following craving induction did not decrease subsequent cue-induced craving or cocaine use.•Blocking the reconsolidation of craving-related memories with pharmacological agents remains an important area of investigation. Cue-induced craving memories, linked to drug-seeking behaviors, require key molecular processes for memory reconsolidation. Lidocaine, a sodium channel blocker, inhibits NMDA receptor activation and suppresses nitric oxide and ERK production. These processes are required for memory re-consolidation; inhibiting them may reduce cue-related craving memories in cocaine dependent subjects. To assess the efficacy of lidocaine in decreasing cue-induced cocaine craving and cocaine use. Treatment-seeking cocaine-dependent participants (n = 33, 25 men) were recruited. Personalized craving and relaxation scripts were developed. Participants were then randomly assigned in a double-blind design to either receive intravenous lidocaine immediately following a cocaine craving script (lidocaine/craving), saline following a craving script (saline/craving), or lidocaine following a relaxation script (lidocaine/relax). One week following the infusion, cue-induced craving was assessed in the same paradigm without an infusion. Cocaine use and craving were assessed for 4 weeks following infusion. The administration of lidocaine during craving induction (lidocaine/craving) did not decrease cue-induced craving during craving reactivation one week later or craving and cocaine use over the 4-week follow-up period compared to the saline/craving group. There were no significant differences in craving and cocaine use between the lidocaine/relax and saline/craving groups. Lidocaine administered following craving induction did not decrease subsequent cue-induced craving or cocaine use. Blocking the reconsolidation of craving-related memories with pharmacological agents remains an important area of investigation.
Cue-induced craving memories, linked to drug-seeking behaviors, require key molecular processes for memory reconsolidation. Lidocaine, a sodium channel blocker, inhibits NMDA receptor activation and suppresses nitric oxide and ERK production. These processes are required for memory re-consolidation; inhibiting them may reduce cue-related craving memories in cocaine dependent subjects. To assess the efficacy of lidocaine in decreasing cue-induced cocaine craving and cocaine use. Treatment-seeking cocaine-dependent participants (n = 33, 25 men) were recruited. Personalized craving and relaxation scripts were developed. Participants were then randomly assigned in a double-blind design to either receive intravenous lidocaine immediately following a cocaine craving script (lidocaine/craving), saline following a craving script (saline/craving), or lidocaine following a relaxation script (lidocaine/relax). One week following the infusion, cue-induced craving was assessed in the same paradigm without an infusion. Cocaine use and craving were assessed for 4 weeks following infusion. The administration of lidocaine during craving induction (lidocaine/craving) did not decrease cue-induced craving during craving reactivation one week later or craving and cocaine use over the 4-week follow-up period compared to the saline/craving group. There were no significant differences in craving and cocaine use between the lidocaine/relax and saline/craving groups. Lidocaine administered following craving induction did not decrease subsequent cue-induced craving or cocaine use. Blocking the reconsolidation of craving-related memories with pharmacological agents remains an important area of investigation.
Cue-induced craving memories, linked to drug-seeking behaviors, require key molecular processes for memory reconsolidation. Lidocaine, a sodium channel blocker, inhibits NMDA receptor activation and suppresses nitric oxide and ERK production. These processes are required for memory re-consolidation; inhibiting them may reduce cue-related craving memories in cocaine dependent subjects.RATIONALCue-induced craving memories, linked to drug-seeking behaviors, require key molecular processes for memory reconsolidation. Lidocaine, a sodium channel blocker, inhibits NMDA receptor activation and suppresses nitric oxide and ERK production. These processes are required for memory re-consolidation; inhibiting them may reduce cue-related craving memories in cocaine dependent subjects.To assess the efficacy of lidocaine in decreasing cue-induced cocaine craving and cocaine use.OBJECTIVESTo assess the efficacy of lidocaine in decreasing cue-induced cocaine craving and cocaine use.Treatment-seeking cocaine-dependent participants (n = 33, 25 men) were recruited. Personalized craving and relaxation scripts were developed. Participants were then randomly assigned in a double-blind design to either receive intravenous lidocaine immediately following a cocaine craving script (lidocaine/craving), saline following a craving script (saline/craving), or lidocaine following a relaxation script (lidocaine/relax). One week following the infusion, cue-induced craving was assessed in the same paradigm without an infusion. Cocaine use and craving were assessed for 4 weeks following infusion.METHODSTreatment-seeking cocaine-dependent participants (n = 33, 25 men) were recruited. Personalized craving and relaxation scripts were developed. Participants were then randomly assigned in a double-blind design to either receive intravenous lidocaine immediately following a cocaine craving script (lidocaine/craving), saline following a craving script (saline/craving), or lidocaine following a relaxation script (lidocaine/relax). One week following the infusion, cue-induced craving was assessed in the same paradigm without an infusion. Cocaine use and craving were assessed for 4 weeks following infusion.The administration of lidocaine during craving induction (lidocaine/craving) did not decrease cue-induced craving during craving reactivation one week later or craving and cocaine use over the 4-week follow-up period compared to the saline/craving group. There were no significant differences in craving and cocaine use between the lidocaine/relax and saline/craving groups.RESULTSThe administration of lidocaine during craving induction (lidocaine/craving) did not decrease cue-induced craving during craving reactivation one week later or craving and cocaine use over the 4-week follow-up period compared to the saline/craving group. There were no significant differences in craving and cocaine use between the lidocaine/relax and saline/craving groups.Lidocaine administered following craving induction did not decrease subsequent cue-induced craving or cocaine use. Blocking the reconsolidation of craving-related memories with pharmacological agents remains an important area of investigation.CONCLUSIONLidocaine administered following craving induction did not decrease subsequent cue-induced craving or cocaine use. Blocking the reconsolidation of craving-related memories with pharmacological agents remains an important area of investigation.
Rational: Cue-induced craving memories, linked to drug-seeking behaviors, require key molecular processes for memory reconsolidation. Lidocaine, a sodium channel blocker, inhibits NMDA receptor activation and suppresses nitric oxide and ERK production. These processes are required for memory re-consolidation; inhibiting them may reduce cue-related craving memories in cocaine dependent subjects. Objectives: To assess the efficacy of lidocaine in decreasing cue-induced cocaine craving and cocaine use. Methods: Treatment-seeking cocaine-dependent participants (n = 33, 25 men) were recruited. Personalized craving and relaxation scripts were developed. Participants were then randomly assigned in a double-blind design to either receive intravenous lidocaine immediately following a cocaine craving script (lidocaine/craving), saline following a craving script (saline/craving), or lidocaine following a relaxation script (lidocaine/relax). One week following the infusion, cue-induced craving was assessed in the same paradigm without an infusion. Cocaine use and craving were assessed for 4 weeks following infusion. Results: The administration of lidocaine during craving induction (lidocaine/craving) did not decrease cue-induced craving during craving reactivation one week later or craving and cocaine use over the 4-week follow-up period compared to the saline/craving group. There were no significant differences in craving and cocaine use between the lidocaine/relax and saline/craving groups. Conclusion: Lidocaine administered following craving induction did not decrease subsequent cue-induced craving or cocaine use. Blocking the reconsolidation of craving-related memories with pharmacological agents remains an important area of investigation.
ArticleNumber 108062
Author Price, Julianne L.
Becker, Josh E.
Leonard, David
Adinoff, Bryon
Shaw, Meredith
Brown, E Sherwood
Kroener, Sven
Suris, Alina
Kandil, Enas
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  surname: Adinoff
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Keywords Cocaine
Lidocaine
Memory reconsolidation
Craving
Language English
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Snippet •Lidocaine, a sodium channel blocker, inhibits NMDA receptor activation and suppresses nitric oxide and ERK production, which are crucial for memory...
Cue-induced craving memories, linked to drug-seeking behaviors, require key molecular processes for memory reconsolidation. Lidocaine, a sodium channel...
Rational: Cue-induced craving memories, linked to drug-seeking behaviors, require key molecular processes for memory reconsolidation. Lidocaine, a sodium...
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StartPage 108062
SubjectTerms Activation
Adult
Animals
Blocking
Cocaine
Cocaine - administration & dosage
Cocaine - adverse effects
Cocaine-Related Disorders - drug therapy
Cocaine-Related Disorders - psychology
Craving
Cues
Double-Blind Method
Drug abuse
Drug-Seeking Behavior - drug effects
Drug-Seeking Behavior - physiology
Efficacy
Female
Glutamic acid receptors (ionotropic)
Health services utilization
Help seeking behavior
Humans
Induced
Induction
Intravenous administration
Lidocaine
Lidocaine - therapeutic use
Male
Memories
Memory
Memory Consolidation - drug effects
Memory Consolidation - physiology
Memory reconsolidation
Men
Middle Aged
N-Methyl-D-aspartic acid receptors
Nitric oxide
Receptor mechanisms
Relaxation
Scripts
Sodium
Treatment Outcome
Voltage-Gated Sodium Channel Blockers - therapeutic use
Title The Efficacy of Lidocaine in Disrupting Cocaine Cue-Induced Memory Reconsolidation
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https://www.ncbi.nlm.nih.gov/pubmed/32480252
https://www.proquest.com/docview/2434257043
https://www.proquest.com/docview/2408843927
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