Rustay Nathan R, Wrenn Craige C, Kinney Jefferson W, Holmes Andrew, Bailey Kathleen R, Sullivan Timothy L, Harris Ashley P, Long Katharine C, Saavedra Maria C, Starosta Grzegorz, Innerfield Caitlin E, Yang Rebecca J, Dreiling Jennifer L, Crawley Jacqueline N
Laboratory of Behavioral Neuroscience, National Institute of Mental Health, Bethesda, MD 20892, USA.
Neuropeptides. 2005 Jun;39(3):239-43. doi: 10.1016/j.npep.2004.12.026.
Galanin (GAL) impairs performance on cognitive tasks when administered centrally to rats. GAL transgenic (GAL-tg) mice overexpressing endogenous GAL show deficits on the probe trial of the Morris water maze spatial learning task, on the social transmission of food preference olfactory memory task, and on the trace cued fear conditioning emotional learning and memory task. Knockout mice deficient in the GAL-R1 receptor subtype were normal on most memory tasks, while showing a small deficit in trace cued fear conditioning, suggesting a selective role for the GAL-R1 in aversive memories, and implicating other GAL receptor subtypes in spatial learning and olfactory social memory. The growing body of rodent literature implicating excess GAL in cognitive impairment is relevant to the overexpression of GAL in the basal forebrain during the progression of Alzheimer's disease.
向大鼠中枢给药时,甘丙肽(GAL)会损害其认知任务表现。过表达内源性甘丙肽的甘丙肽转基因(GAL-tg)小鼠在莫里斯水迷宫空间学习任务的探针试验、食物偏好嗅觉记忆任务的社会传递以及痕迹线索恐惧条件反射情绪学习和记忆任务中均表现出缺陷。缺乏GAL-R1受体亚型的基因敲除小鼠在大多数记忆任务中表现正常,但在痕迹线索恐惧条件反射中表现出轻微缺陷,这表明GAL-R1在厌恶记忆中具有选择性作用,并暗示其他GAL受体亚型在空间学习和嗅觉社会记忆中发挥作用。越来越多的啮齿动物文献表明过量的甘丙肽与认知障碍有关,这与阿尔茨海默病进展过程中基底前脑甘丙肽的过表达有关。