ω-3PUFAs prevent MK-801-induced cognitive impairment in schizophrenic rats via the CREB/BDNF/TrkB pathway

• DOI: 10.1007/s11596-017-1762-4
• Publication Date: 2018-01-08T22:09:40Z
• Authors: Mao-sheng Fang; Xing Li; Hong Qian; Kuan Zeng; Meng Ye; Yong-jie Zhou; Hui Li; Xiao-chuan Wang; Yi Li
• Keywords: Neurons; Brain-Derived Neurotrophic Factor; Spatial Learning; Cell Count; Hippocampus; Rats, Sprague-Dawley; 03 medical and health sciences; 0302 clinical medicine; Fatty Acids, Omega-3; Schizophrenia; Animals; Receptor, trkB; Cognitive Dysfunction; Dizocilpine Maleate; Phosphorylation; Cyclic AMP Response Element-Binding Protein; Extracellular Signal-Regulated MAP Kinases; Proto-Oncogene Proteins c-akt; Signal Transduction

This study was to determine the protective effect of ω-3 polyunsaturated fatty acids (ω-3PUFAs) on MK-801-induced cognitive impairment in schizophrenia (SZ) rats and the underlying mechanism. A rat model of schizophrenia was induced by MK-801. The cognitive function of rats was assessed using a Morris water maze. The number of hippocampal neurons was measured by Nissl staining. The expression of CREB, p-CREB, BDNF, TrkB, p-TrkB, AKT, p-AKT, ERK, and p-ERK in the hippocampus of rats was detected by Western blotting. The results showed that ω-3PUFAs attenuated MK-801-induced cognitive impairment and hippocampal neurons loss, reversed the injury of the CREB/BDNF/TrkB pathway induced by MK-801, and antagonized MK-801-induced down-regulation of p-AKT and p-ERK in the hippocampus of rats. In conclusion, ω-3PUFAs enhances the CREB/BDNF/TrkB pathway by activating ERK and AKT, thereby increasing the synaptic plasticity and decreasing neuron loss, and antagonizing MK-801-induced cognitive impairment in schizophrenic rats.