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Objective Depression is a common mental disorder with high prevalence, high disability rate and high suicide rate, and severely impairs human lives and health.Recent studies have shown that depression has a close relationship with abnormal hippocampal neuroplasticity.Reversing this process is thought to be a new strategy for rapid antidepression.Finding the key moleculars that regulate this kind of hippocampal neuroplasticity is expected to find candidate targets for antidepressants.Howerver, little is known about the molecular mechanism for antidepressants regulating neuroplasticity.The present research aimed at exploring whether Bcl-2/adenovirus E1B 19 kD-interacting protein 3 (BNIP3) participates in antidepression by regulating the hippocampal neuroplasticity, providing experimental evidences for finding candidate and rapid antidepressant targets for depression treatment.Methods The expression of BNIP3 is quantified by real-time PCR and western blot during the key period of the development of the dendrite, spine and synapse formation of hippocampal neuron.Overexpression of BNIP3 and RNA interference methods were used to determine the influence of BNIP3 on dendrite arbors of hippoeampal neuron.Using real-time PCR and western blot methods to quantify the expression of BNIP3, synapsinI and GIuRI after the administration of imipramine and fluoxetine.Results (1) BNIP3 continued to increase during the critical period of the dendrite, spine and synapse formation of hippocampal neuron in culture.(2) Antidepressants imipramine and fluoxetine could increase the expression of BNIP3, synapsinI and GluRI in hippocampal neuron.(3) Overexpression ofBNIP3 increased the number of dendrite arbors of hippocampal neuron, while BNIP3 siRNA has no influence on the number of dendrite arbors of hippocampal neuron.Conclusion BNIP3 may participate in the antidepressants effects on the hippocampal neuroplasticity.