title: Effects of Sodium Benzoate Treatment in Combination with An Extinction Training on the Maintenance of Cocaine-Supported Memory.
abstract: 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 cocaine-induced 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 cocaine-supported memory. Moreover, systemic NaB treatment exerts such effects, at least in part, via its effect in the mPFC.
authors.affiliation: Institute of Behavioral Medicine, National Cheng Kung University College of Medicine, Tainan 70101, Taiwan, Republic of China.
authors.forename: Yi-Ni
authors.initials: YN
authors.lastname: Tsai
authors.affiliation: Institute of Behavioral Medicine, National Cheng Kung University College of Medicine, Tainan 70101, Taiwan, Republic of China.
authors.forename: Wen-Yu
authors.initials: WY
authors.lastname: Tzeng
authors.affiliation: Department of Health Psychology, Chang Jung Christian University, Tainan 71101, Taiwan, Republic of China.
authors.forename: Chianfang G
authors.initials: CG
authors.lastname: Cherng
authors.affiliation: Institute of Behavioral Medicine, National Cheng Kung University College of Medicine, Tainan 70101, Taiwan, Republic of China.
authors.forename: Tien You
authors.initials: TY
authors.lastname: Liao
authors.affiliation: Institute of Behavioral Medicine, National Cheng Kung University College of Medicine, Tainan 70101, Taiwan, Republic of China.
authors.forename: Hsin-Hua
authors.initials: HH
authors.lastname: Wu
authors.affiliation: Department of Physiology, National Cheng Kung University College of Medicine, Tainan 70101, Taiwan, Republic of China.
authors.forename: Jie-Kuan
authors.initials: JK
authors.lastname: Lin
authors.affiliation: Institute of Behavioral Medicine, National Cheng Kung University College of Medicine, Tainan 70101, Taiwan, Republic of China.|Department of Physiology, National Cheng Kung University College of Medicine, Tainan 70101, Taiwan, Republic of China.
authors.forename: Lung
authors.initials: L
authors.lastname: Yu
mesh_terms: D000818:Animals; D003042:Cocaine / Q000494:pharmacology*; D003213:Conditioning, Psychological / Q000187:drug effects; D005108:Extinction, Psychological; D008297:Male; D008568:Memory / Q000187:drug effects*; D051379:Mice; D017397:Prefrontal Cortex / Q000187:drug effects / Q000502:physiology; D020160:Sodium Benzoate / Q000494:pharmacology*
chemical_list: D003042:Cocaine; D020160:Sodium Benzoate