Frontiers in Pharmacology · 2018 · 51 citations · 21 references
MedicineNeurosciencePharmacologyBehavioral PharmacologyMemoryNeuropharmacologyCognitive ImpairmentHippocampal SystemsMemory In AnimalsNeural Basis Of MemoryNeuroprotectionNeuroprotective PharmacologyCholinergic Modulation Of CognitionCholinergic Modulation Of MemoryCognitive EffectsCognitive Enhancement By Cholinergic AgentsIntraperitoneal AdministrationPretreatmentRodent MemoryRodent Neuropharmacology
seed extract (MSE) on cognitive impairment caused by scopolamine injection in mice using the passive avoidance and Morris water maze (MWM) tests. MSE (250 or 500 mg/kg) was administered to mice by oral gavage for 7 or 14 days, and cognitive impairment was induced by intraperitoneal injection of scopolamine (4 mg/kg) for 1 or 6 days. Mice that received scopolamine alone showed impaired learning and memory retention and considerably decreased cholinergic system reactivity and neurogenesis in the hippocampus. MSE pretreatment significantly ameliorated scopolamine-induced cognitive impairment and enhanced cholinergic system reactivity and neurogenesis in the hippocampus. Additionally, the protein expressions of phosphorylated Akt, ERK1/2, and CREB in the hippocampus were significantly decreased by scopolamine, but these decreases were reversed by MSE treatment. These results suggest that MSE-induced ameliorative cognitive effects are mediated by enhancement of the cholinergic neurotransmission system and neurogenesis via activation of the Akt, ERK1/2, and CREB signaling pathways. These findings suggest that MSE could be a potent neuropharmacological drug against amnesia, and its mechanism might be modulation of cholinergic activity via the Akt, ERK1/2, and CREB signaling pathways.
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