Chronic antidepressant treatment increases neurogenesis in the adult rat hippocampus. This study used bromodeoxyuridine (BrdU) to label dividing cells and found that chronic antidepressant treatment significantly increased the number of BrdU-labeled cells in the dentate gyrus and hilus of the hippocampus. Administration of various antidepressants, but not non-antidepressants, increased BrdU-labeled cells, indicating a common and selective effect of antidepressants. Antidepressants also increased the proliferation of hippocampal cells, which mature into neurons. These findings suggest that increased cell proliferation and neuronal number may be a mechanism by which antidepressants counteract stress-induced atrophy and loss of hippocampal neurons, contributing to their therapeutic effects. Depression affects 12–17% of the population and is associated with hippocampal atrophy. Stress can reduce hippocampal neurogenesis, and antidepressants may counteract this. The hippocampus is one of the few brain regions where neurogenesis occurs throughout life. Stress suppresses hippocampal granule cell formation, and chronic stress reduces cell proliferation. Antidepressants increase BrdU labeling, indicating increased cell proliferation and neurogenesis. This may help reverse stress-induced hippocampal atrophy. Antidepressants increase BrdU labeling in the hippocampus, with effects observed after chronic treatment. Fluoxetine, tranylcypromine, and reboxetine increased BrdU-labeled cells. The increase was not seen with acute treatment. Antidepressants also increased the survival of BrdU-labeled cells, suggesting that they enhance both proliferation and survival of hippocampal cells. These cells mature into neurons, as shown by triple labeling with BrdU and neuronal or glial markers. Antidepressants increase neurogenesis in the hippocampus, with new cells surviving and differentiating into neurons. This is supported by findings that antidepressants increase BrdU labeling and that the majority of BrdU-positive cells are neurons. Antidepressants do not affect the differentiation of cells into neurons or glia. The survival of newly born cells in the hippocampus is not significantly affected by antidepressants, but their proliferation is increased. The study suggests that antidepressants may enhance hippocampal neurogenesis, which could contribute to their therapeutic effects in depression. This is consistent with the time course of antidepressant action and the observed increase in BrdU labeling. The findings indicate that antidepressants may counteract stress-induced hippocampal atrophy and improve hippocampal function. Future studies are needed to determine if these effects occur in humans and whether they contribute to the therapeutic response to antidepressants.Chronic antidepressant treatment increases neurogenesis in the adult rat hippocampus. This study used bromodeoxyuridine (BrdU) to label dividing cells and found that chronic antidepressant treatment significantly increased the number of BrdU-labeled cells in the dentate gyrus and hilus of the hippocampus. Administration of various antidepressants, but not non-antidepressants, increased BrdU-labeled cells, indicating a common and selective effect of antidepressants. Antidepressants also increased the proliferation of hippocampal cells, which mature into neurons. These findings suggest that increased cell proliferation and neuronal number may be a mechanism by which antidepressants counteract stress-induced atrophy and loss of hippocampal neurons, contributing to their therapeutic effects. Depression affects 12–17% of the population and is associated with hippocampal atrophy. Stress can reduce hippocampal neurogenesis, and antidepressants may counteract this. The hippocampus is one of the few brain regions where neurogenesis occurs throughout life. Stress suppresses hippocampal granule cell formation, and chronic stress reduces cell proliferation. Antidepressants increase BrdU labeling, indicating increased cell proliferation and neurogenesis. This may help reverse stress-induced hippocampal atrophy. Antidepressants increase BrdU labeling in the hippocampus, with effects observed after chronic treatment. Fluoxetine, tranylcypromine, and reboxetine increased BrdU-labeled cells. The increase was not seen with acute treatment. Antidepressants also increased the survival of BrdU-labeled cells, suggesting that they enhance both proliferation and survival of hippocampal cells. These cells mature into neurons, as shown by triple labeling with BrdU and neuronal or glial markers. Antidepressants increase neurogenesis in the hippocampus, with new cells surviving and differentiating into neurons. This is supported by findings that antidepressants increase BrdU labeling and that the majority of BrdU-positive cells are neurons. Antidepressants do not affect the differentiation of cells into neurons or glia. The survival of newly born cells in the hippocampus is not significantly affected by antidepressants, but their proliferation is increased. The study suggests that antidepressants may enhance hippocampal neurogenesis, which could contribute to their therapeutic effects in depression. This is consistent with the time course of antidepressant action and the observed increase in BrdU labeling. The findings indicate that antidepressants may counteract stress-induced hippocampal atrophy and improve hippocampal function. Future studies are needed to determine if these effects occur in humans and whether they contribute to the therapeutic response to antidepressants.