OBJECTIVEThe 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.

METHODSAdult 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.

RESULTSThe 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.

CONCLUSIONThis may have clinic application in preventing hippocampal damage after glucocorticoid treatment.

Analysis of Variance ; Animals ; Bromodeoxyuridine ; metabolism ; Cell Count ; Cell Proliferation ; drug effects ; Corticosterone ; pharmacology ; Drug Interactions ; Hippocampus ; cytology ; Male ; Neural Inhibition ; drug effects ; Neurons ; drug effects ; Paroxetine ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Serotonin Uptake Inhibitors ; pharmacology