Hippocampal proteomic changes in a rat model of depression induced by dexamethasone
Keywords:
Proteomic analysis, Depression, Hippocampus, Dexamethasone, Synaptic dysfunctionAbstract
This study aimed to examine possible alterations of protein expression in the hippocampus of a rat model of depression induced by dexamethasone using the proteomic technique. The altered expression of several proteins has been found in a depressive group. The identified proteins play an important role in the cell signalling process, consisting of serotonergic, norepinephrinergic, dopaminergic, glutamatergic, and GABAergic receptors, the synaptic signalling associated proteins and the protein markers of GABAergic system. These results indicate the abnormality of signal transduction processes and the neurotransmitter dysfunction in depression. Moreover, up-regulation of beta-nerve growth factor, a neurotrophic factor involved in the survival of neurons, and down-regulation of amyloid-beta A4 precursor protein-binding family A member 1, a protein involved in the processing of the amyloid-beta precursor protein and signal transduction processes, were found in the depressive group. These findings reveal that the identified proteins in the hippocampus of the depressive model are important in the synaptic transmission process. It also shows synaptic dysfunction in depression. In summary, the identified proteins in this study by the proteomics technique could be used as the protein markers for further investigation.
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