Kopf S R, Boccia M M, Baratti C M
Laboratorio de Neurofarmacología de Procesos de Memoria, Cátedra de Farmacología-Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Junín 956-5 degrees Piso, Buenos Aires, 1113, Argentina.
Neurobiol Learn Mem. 1998 Nov;70(3):305-13. doi: 10.1006/nlme.1998.3855.
Male Swiss mice were tested 24 h after training in a one-trial step-through inhibitory avoidance task. Low subeffective doses of d-(+)-glucose (10 mg/kg, ip), but not its stereoisomer l-(-)-glucose (30 mg/kg,ip), administered immediately after training, and AF-DX 116 (0.3 mg/kg,ip), a presynaptic muscarinic receptor antagonist, given 10 min after training, interact to improve retention. Insulin (8 IU/kg, ip) impaired retention when injected immediately after training, and the effects were reversed, in a dose-related manner, by AF-DX 116 (0.3, 1.0, or 3.0 mg/kg, ip) administered 10 min following insulin. Since AF-DX 116 possibly blocks autoreceptors mediating the inhibition of acetylcholine release from cholinergic nerve terminals, the present data support the view that changes in the central nervous system glucose availability, subsequent to modification of circulating glucose levels, influence the activity of central cholinergic mechanisms involved in memory storage of an inhibitory avoidance response in mice.
在单次尝试的穿梭式抑制性回避任务训练24小时后，对雄性瑞士小鼠进行测试。训练后立即给予低亚有效剂量的d-(+)-葡萄糖（10毫克/千克，腹腔注射），而非其立体异构体l-(-)-葡萄糖（30毫克/千克，腹腔注射），以及训练后10分钟给予的突触前毒蕈碱受体拮抗剂AF-DX 116（0.3毫克/千克，腹腔注射），它们相互作用可改善记忆保持。训练后立即注射胰岛素（8国际单位/千克，腹腔注射）会损害记忆保持，而在胰岛素注射10分钟后给予AF-DX 116（0.3、1.0或3.0毫克/千克，腹腔注射），其作用会以剂量相关的方式逆转。由于AF-DX 116可能阻断介导抑制胆碱能神经末梢乙酰胆碱释放的自身受体，目前的数据支持这样一种观点，即在循环葡萄糖水平改变后，中枢神经系统葡萄糖可用性的变化会影响参与小鼠抑制性回避反应记忆存储的中枢胆碱能机制的活性。
