Betaine (trimethylglycine) is a neutral chemical compound found naturally in many plants. Recently, we have found that betaine potentially acts on glycine binding site of NMDA receptor as a partial agonist. NMDA receptor glycine binding site agonist and partial agonists have been reported to accelerate extinction of drug seeking behavior. The present study aimed to determine whether betaine facilitates extinction of methamphetamine (MA) and morphine (MOR) conditioned place preference (CPP). After MA/MOR CPP, rats received betaine (100 mg/kg) or saline immediately after con fi ned extinction, with saline injection in previous MA-paired compartment for 3 days. MA CPP was significantly reduced during retest after extinction in rats treated with saline and betaine, but MA priming induced reinstatement in the saline-treated, but not betaine-treated rats. MOR CPP was effectively extinct in betaine- , but not saline-treated rats. The MOR priming did not induce reinstatement in the betaine-treated rats. In addition, after complete extinction, acute betaine treatment 30 min prior to MA/MOR priming injection significantly reduced the reinstatement. These results demonstrated that betaine facilitates memory consolidation for extinction of approach behavior to environmental stimuli previously paired with MA/MOR and suppresses MA/MOR-induced reinstatement of CPP behavior, suggesting that betaine is a potential therapeutic agent for MA/MOR addiction.
Date:
2014-08
Relation:
Journal of Neurochemistry. 2014 Aug;130(Suppl. s1):63.
