Gongjin-Dan Enhances Hippocampal Memory in a Mouse Model of Scopolamine-Induced Amnesia

• Published in: PloS one 2016-08, Vol.11 (8), p.e0159823-e0159823
• Main Authors: Lee, Jin-Seok, Hong, Sung-Shin, Kim, Hyeong-Geug, Lee, Hye-Won, Kim, Won-Yong, Lee, Sam-Keun, Son, Chang-Gue
• Format: Article
• Language: English
• Subjects: Acetylcholinesterase; Acetylcholinesterase - metabolism; Alzheimer's disease; Amnesia; Amnesia - chemically induced; Amnesia - drug therapy; Amnesia - metabolism; Amnesia - physiopathology; Analysis; Animals; Atrophy; Avoidance; Avoidance Learning - drug effects; Biology and Life Sciences; Brain; Brain research; Brain-derived neurotrophic factor; Brain-Derived Neurotrophic Factor - analysis; Brain-Derived Neurotrophic Factor - metabolism; Care and treatment; Cell Line; Chromatography; Disease Models, Animal; Doublecortin protein; Drug dosages; Growth factors; Health aspects; Hippocampus; Hippocampus - drug effects; Hippocampus - metabolism; Hippocampus - physiopathology; Immunology; Influence; Latency; Learning; Liver; Male; Maze Learning - drug effects; Medicine and Health Sciences; Memory; Memory - drug effects; Mice; Mice, Inbred BALB C; Nerve growth factor; Nerve Growth Factor - analysis; Nerve Growth Factor - metabolism; Neurogenesis; Pharmacy; Plant Extracts - therapeutic use; Receptors; Research and Analysis Methods; Rodents; Scopolamine; Scopolamine Hydrobromide; Short term memory; Staining; Tacrine; Traditional medicine
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0159823

We evaluated the neuropharmacological effects of Gongjin-Dan (GJD) on the memory impairment caused by scopolamine injection. BALB/c mice were orally treated with GJD (100, 200, or 400 mg/kg, daily) or tacrine (THA, 10 mg/kg) for 10 days, and scopolamine (2 mg/kg) was injected intraperitoneally. The radial arm maze and passive avoidance tests were performed to evaluate the animal's learning and memory. Scopolamine increased the task completing time, the number of total errors (reference and working memory error) in the radial arm maze task, and the latency time in the passive avoidance test, which were significantly ameliorated by treatment with GJD. The GJD treatment also attenuated the scopolamine-induced hyperactivation of acetylcholinesterase activity, and suppression of the expression of brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF) and their receptors in the hippocampus. These effects of GJD were supported by both the doublecortin (DCX)-positive staining and Nissl staining, which were used to measure hippocampal neurogenesis and atrophy, respectively. These findings strongly suggest that GJD exerts a potent anti-amnesic effect, and its underlying mechanism might involve the modulation of cholinergic activity.