Ervin G N, Birkemo L S, Johnson M F, Conger L K, Mosher J T, Menius J A
Department of Pharmacology, Glaxo Research Institute, Research Triangle Park, North Carolina, USA.
J Pharmacol Exp Ther. 1995 Jun;273(3):1203-10.
We compared the effects of intraperitoneally administered LiCl (0.5-2830 mumol/kg), sulfated cholecystokinin26-33 (10-1000 nmol/kg; CCK-8), nonsulfated CCK-8 (500 and 1000 nmol/kg), sulfated CCK26-29 (500 and 1000 nmol/kg), CCK30-33 (10-1000 nmol/kg) bombesin (10-1000 nmol/kg; BOM), (dl) fenfluramine HCl (0.9-37.3 mumol/kg; fenfluramine), fluoxetine HCl (2.9-86.7 mumol/kg; fluoxetine), and d-amphetamine sulfate (0.27-10.9 mumol/kg; AMPH) on both 18-hr deprivation-induced feeding and one-bottle, taste aversion conditioning in male, Long-Evans rats. Doses of LiCl > or = 177 mumol/kg (or 7.5 mg/kg) induced significant, dose-related taste aversions, but only doses of LiCl > or = 2123 mumol/kg (90 and 120 mg/kg) induced significant anorexia. CCK-8 induced marked anorexia (at doses > or = 25-50 nmol/kg), but only relatively mild taste aversions which were only statistically significant at the highest dose (1000 nmol/kg). The anorectic effects of CCK-8 at 500 and 1000 nmol/kg, but not at lower doses, lasted at least 3 hr. Sulfated CCK26-29, CCK30-33 and nonsulfated CCK-8 induced neither anorexia nor taste aversion. BOM induced marked anorexia at all doses tested, but did not induce statistically significant taste aversions. The nonpeptidal anorectic compounds, fenfluramine, fluoxetine, and AMPH, induced both dose-related anorexia and taste aversion conditioning. We focus on several issues concerning the interpretation of taste aversion conditioning. Our results challenge any simple relationship between the ability of a compound to induce taste aversion and to decrease feeding.
我们比较了腹腔注射氯化锂（0.5 - 2830微摩尔/千克）、硫酸化胆囊收缩素26 - 33（10 - 1000纳摩尔/千克；CCK - 8）、非硫酸化CCK - 8（500和1000纳摩尔/千克）、硫酸化CCK26 - 29（500和1000纳摩尔/千克）、CCK30 - 33（10 - 1000纳摩尔/千克）、蛙皮素（10 - 1000纳摩尔/千克；BOM）、（消旋）盐酸芬氟拉明（0.9 - 37.3微摩尔/千克；芬氟拉明）、盐酸氟西汀（2.9 - 86.7微摩尔/千克；氟西汀）和硫酸右苯丙胺（0.27 - 10.9微摩尔/千克；AMPH）对雄性Long - Evans大鼠18小时禁食诱导的进食以及单瓶味觉厌恶条件反射的影响。剂量≥177微摩尔/千克（或7.5毫克/千克）的氯化锂可诱导显著的、与剂量相关的味觉厌恶，但只有剂量≥2123微摩尔/千克（90和120毫克/千克）的氯化锂可诱导显著的厌食。CCK - 8可诱导明显的厌食（剂量≥25 - 50纳摩尔/千克时），但仅引起相对较轻的味觉厌恶，且仅在最高剂量（1000纳摩尔/千克）时具有统计学意义。500和1000纳摩尔/千克的CCK - 8的厌食作用持续至少3小时，但较低剂量时无此作用。硫酸化CCK26 - 29、CCK30 - 33和非硫酸化CCK - 8既不诱导厌食也不诱导味觉厌恶。BOM在所有测试剂量下均诱导明显的厌食，但未诱导出具有统计学意义的味觉厌恶。非肽类厌食化合物芬氟拉明、氟西汀和AMPH可诱导与剂量相关的厌食和味觉厌恶条件反射。我们关注了几个与味觉厌恶条件反射解释相关的问题。我们的结果对化合物诱导味觉厌恶和减少进食能力之间的任何简单关系提出了挑战。
