QBI Seminar: Neurotrophic Factor α-1 - A Key Regulator of Neuroprotection and Depression during Stress
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- Dr Y-Peng Loh
Chief, Section on Cellular Neurobiology, Eunice Kennedy Shriver National Institutes of Child Health and Human Development, National Institutes of Health, Bethesda, USA
Title: Neurotrophic Factor α-1 : A Key Regulator of Neuroprotection and Depression during Stress
Abstract:
Neurotrophic factor α-1 (NF α-1, also known as Carboxypeptidase E) is a signaling molecule that is highly expressed in the CA3 region of the hippocampus and acts extracellularly in neuroprotection and prevention of depression during chronic stress.
Mice lacking NF α-1 exhibit neuronal degeneration in the hippocampal CA3 region and depression. Pretreatment of rat hippocampal neurons with purified NF α-1 protected the cells against H2O2, glutamate and amyloid beta 1-42 induced cell death. The neuroprotective signaling pathways of NF α-1 involved the activation of the ERK and Akt pathways which induced the expression of the anti-apoptotic mitochondrial protein, Bcl-2. In vivo, mice subjected to chronic stress showed co-ordinate increase in NF α-1 Akt phosphorylation and Bcl-2 expression to mediate neuroprotection in the hippocampus. We also showed that FGF2 mRNA and protein levels were significantly reduced in the hippocampus of NF α-1-KO mice which were severely depressed by the forced swim assay, compared to WT littermates. This is consistent with FGF2 being very low in post mortem brains of depressed patients. FGF2 has been shown to be a anti-depressant in rodents. I.p. injection of FGF2 completely rescued the NF α-1-KO mice from depression through induced neurogenesis in the hippocampus. Short term chronic stress of mice induced NF α-1 and FGF2 expression, which then resulted in enhanced neurogenesis in the hippocampus, thereby preventing the onset of depressive-like behavior. However, long term chronic stress did precipitate depression. Thus, NF α-1 plays a key role in neuroprotection and preventing depression during short term chronic stress.
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