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題名 Lamotrigine attenuates the motivation to self-administer ketamine and prevents cue- and prime-induced reinstatement of ketamine-seeking behavior in rats
作者 詹銘煥
Lee, Mei-Yi
Hsiao, Yu-Ching
Chan, Ming-Huan
貢獻者 神科所
關鍵詞 Breakpoint; Extinction; Locomotor activity; Progressive ratio; Relapse
日期 2018-08
上傳時間 16-一月-2019 17:28:42 (UTC+8)
摘要 BACKGROUND:Lamotrigine is an anticonvulsant drug used in the treatment of epilepsy and bipolar disorder. A case report has demonstrated that a ketamine addict experienced a significant reduction in craving and ketamine use after taking lamotrigine. The present study determined whether lamotrigine can reduce the motivation for ketamine and prevent the relapse to ketamine seeking behavior in rats.METHODS:Male Sprague-Dawley rats were trained to respond for intravenous ketamine (0.5 mg/kg/infusion) self-administration or food pellets. The effects of lamotrigine on the motivation for ketamine or food were assessed using breakpoint test under a progressive ratio (PR) paradigm. Furthermore, the effects of lamotrigine on reinstatement of ketamine-seeking and food-seeking behaviors were examined after extinction.RESULTS:Lamotrigine significantly decreased the breakpoint for ketamine and prevented cue- and ketamine priming-induced reinstatement of ketamine seeking behavior. However, lamotrigine did not affect the breakpoint for food reinforcement, cue-induced reinstatement of food-seeking behavior, or spontaneous locomotor activity.CONCLUSIONS:Our data reveal that lamotrigine is capable of attenuating the reinforcing efficacy of ketamine and reducing ketamine craving and relapse risk, which lays the foundation for conducting clinical trials in patients with ketamine use disorder.
關聯 Drug and Alcohol Dependence, Volume 194, 1 January 2019, Pages 257-263
資料類型 article
DOI http://dx.doi.org/10.1016/j.drugalcdep.2018.10.028
dc.contributor 神科所
dc.creator (作者) 詹銘煥
dc.creator (作者) Lee, Mei-Yi
dc.creator (作者) Hsiao, Yu-Ching
dc.creator (作者) Chan, Ming-Huan
dc.date (日期) 2018-08
dc.date.accessioned 16-一月-2019 17:28:42 (UTC+8)-
dc.date.available 16-一月-2019 17:28:42 (UTC+8)-
dc.date.issued (上傳時間) 16-一月-2019 17:28:42 (UTC+8)-
dc.identifier.uri (URI) http://nccur.lib.nccu.edu.tw/handle/140.119/121925-
dc.description.abstract (摘要) BACKGROUND:Lamotrigine is an anticonvulsant drug used in the treatment of epilepsy and bipolar disorder. A case report has demonstrated that a ketamine addict experienced a significant reduction in craving and ketamine use after taking lamotrigine. The present study determined whether lamotrigine can reduce the motivation for ketamine and prevent the relapse to ketamine seeking behavior in rats.METHODS:Male Sprague-Dawley rats were trained to respond for intravenous ketamine (0.5 mg/kg/infusion) self-administration or food pellets. The effects of lamotrigine on the motivation for ketamine or food were assessed using breakpoint test under a progressive ratio (PR) paradigm. Furthermore, the effects of lamotrigine on reinstatement of ketamine-seeking and food-seeking behaviors were examined after extinction.RESULTS:Lamotrigine significantly decreased the breakpoint for ketamine and prevented cue- and ketamine priming-induced reinstatement of ketamine seeking behavior. However, lamotrigine did not affect the breakpoint for food reinforcement, cue-induced reinstatement of food-seeking behavior, or spontaneous locomotor activity.CONCLUSIONS:Our data reveal that lamotrigine is capable of attenuating the reinforcing efficacy of ketamine and reducing ketamine craving and relapse risk, which lays the foundation for conducting clinical trials in patients with ketamine use disorder.en_US
dc.format.extent 408107 bytes-
dc.format.mimetype application/pdf-
dc.relation (關聯) Drug and Alcohol Dependence, Volume 194, 1 January 2019, Pages 257-263
dc.subject (關鍵詞) Breakpoint; Extinction; Locomotor activity; Progressive ratio; Relapseen_US
dc.title (題名) Lamotrigine attenuates the motivation to self-administer ketamine and prevents cue- and prime-induced reinstatement of ketamine-seeking behavior in ratsen_US
dc.type (資料類型) article
dc.identifier.doi (DOI) 10.1016/j.drugalcdep.2018.10.028
dc.doi.uri (DOI) http://dx.doi.org/10.1016/j.drugalcdep.2018.10.028