Effects of sodium benzoate treatment in combination with an extinction training on the maintenance of cocaine-supported memory

Yi Ni Tsai, Wen Yu Tzeng, Chianfang G. Cherng, Tien You Liao, Hsin Hua Wu, Jie Kuan Lin, Lung Yu

研究成果: Article

1 引文 (Scopus)

摘要

Activation of N-methyl-D-aspartate (NMDA) receptor can facilitate the extinction of various maladaptive memories. Sodium benzoate (NaB) has been known to enhance a naturally occurring full agonist on the glycine binding site of the NMDA receptor. This study aimed to test whether systemic NaB treatment can affect the extinction of a cocaine-supported memory, the cocaine-induced conditioned place preference (CPP). Following the establishment of the cocaine (10 mg/kg/conditioning × 3)-induced CPP, an extinction protocol, consisting of two consecutive extinction training bouts at an 8-h interval, was used. NaB (500 mg/kg) or an equivalent volume of saline was given immediately following each extinction training bout to test the modulating effect of NaB on the maintenance of cocaine-induced CPP. Moreover, NaB was bilaterally micro-infused into the medial prefrontal cortex (mPFC) to validate the involvement of this brain region in mediating systemic NaB treatment-produced effect on cocaineinduced CPP. Systemic (500 mg/kg) and intra-mPFC (10 μg/side) NaB treatment significantly decreased subsequent cocaine-induced CPP magnitude, although the NaB treatment or the extinction training alone did not affect such CPP magnitude. It was of importance to note that systemic or intra-mPFC NaB delivery did not affect mouse locomotor activity in the retests. These results, taken together, suggest that NaB treatment in combination with the extinction training may facilitate the extinction of the cocainesupported memory. Moreover, systemic NaB treatment exerts such effects, at least in part, via its effect in the mPFC.

原文English
頁(從 - 到)56-61
頁數6
期刊Chinese Journal of Physiology
59
發行號1
DOIs
出版狀態Published - 2016 一月 1

指紋

Sodium Benzoate
Cocaine
Maintenance
Prefrontal Cortex
N-Methyl-D-Aspartate Receptors
Psychological Extinction
Locomotion
Glycine
Binding Sites

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

引用此文

Tsai, Yi Ni ; Tzeng, Wen Yu ; Cherng, Chianfang G. ; Liao, Tien You ; Wu, Hsin Hua ; Lin, Jie Kuan ; Yu, Lung. / Effects of sodium benzoate treatment in combination with an extinction training on the maintenance of cocaine-supported memory. 於: Chinese Journal of Physiology. 2016 ; 卷 59, 編號 1. 頁 56-61.
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Effects of sodium benzoate treatment in combination with an extinction training on the maintenance of cocaine-supported memory. / Tsai, Yi Ni; Tzeng, Wen Yu; Cherng, Chianfang G.; Liao, Tien You; Wu, Hsin Hua; Lin, Jie Kuan; Yu, Lung.

於: Chinese Journal of Physiology, 卷 59, 編號 1, 01.01.2016, p. 56-61.

研究成果: Article

TY - JOUR

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AU - Tsai, Yi Ni

AU - Tzeng, Wen Yu

AU - Cherng, Chianfang G.

AU - Liao, Tien You

AU - Wu, Hsin Hua

AU - Lin, Jie Kuan

AU - Yu, Lung

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N2 - Activation of N-methyl-D-aspartate (NMDA) receptor can facilitate the extinction of various maladaptive memories. Sodium benzoate (NaB) has been known to enhance a naturally occurring full agonist on the glycine binding site of the NMDA receptor. This study aimed to test whether systemic NaB treatment can affect the extinction of a cocaine-supported memory, the cocaine-induced conditioned place preference (CPP). Following the establishment of the cocaine (10 mg/kg/conditioning × 3)-induced CPP, an extinction protocol, consisting of two consecutive extinction training bouts at an 8-h interval, was used. NaB (500 mg/kg) or an equivalent volume of saline was given immediately following each extinction training bout to test the modulating effect of NaB on the maintenance of cocaine-induced CPP. Moreover, NaB was bilaterally micro-infused into the medial prefrontal cortex (mPFC) to validate the involvement of this brain region in mediating systemic NaB treatment-produced effect on cocaineinduced CPP. Systemic (500 mg/kg) and intra-mPFC (10 μg/side) NaB treatment significantly decreased subsequent cocaine-induced CPP magnitude, although the NaB treatment or the extinction training alone did not affect such CPP magnitude. It was of importance to note that systemic or intra-mPFC NaB delivery did not affect mouse locomotor activity in the retests. These results, taken together, suggest that NaB treatment in combination with the extinction training may facilitate the extinction of the cocainesupported memory. Moreover, systemic NaB treatment exerts such effects, at least in part, via its effect in the mPFC.

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