Objective The literature has shown that cognitive and emotional changes may occur after chronic treatment with glucocorticoids. This might be caused by the suppressive effect of glucocorticoids on hippocampal neurogenesis and cell proliferation. Paroxetine, a selective serotonin reuptake transporter, is a commonly used antidepressant for alleviation of signs and symptoms of clinical depression. It was discovered to promote hippocampal neurogenesis in the past few years and we wanted to investigate its interaction with glucocorticoid in this study. Methods Adult rats were given vehicle, corticosterone, paroxetine, or both corticosterone and paroxetine for 14 d. Cell proliferation in the dentate gyrus was quantified using 5-bromo-2-deoxyuridine （BrdU） immunohistochemistry. Results The corticosterone treatment suppressed while paroxetine treatment increased hippocampal cell proliferation. More importantly, paroxetine treatment could reverse the suppressive effect of corticosterone on hippocampal cell proliferation. Conclusion This may have clinic application in preventing hippocampal damage after glucocorticoid treatment.
The benefits of dietary restriction （DR） on health and aging prevention have been well recognized. Recent studies suggest that DR may enhance brain functions including learning and memory, synaptic plasticity, and neurogenesis, all of which are associated with brain health. Under the stress stimulated by DR, a favorable environment is established for facilitating neuronal plasticity, enhancing cognitive function, stimulating neurogenesis and regulating inflammatory response. DR-induced expressions of factors such as heat shock proteins （HSPs）, neurotrophic factors, and Sirtuin1 （SIRT1） are responsible for the effect of DR on the brain. Due to the difficulty in practising long-term DR in human, the potential mimics of DR are also discussed.
