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Karger AG","issue":"1","license":[{"start":{"date-parts":[[2019,1,1]],"date-time":"2019-01-01T00:00:00Z","timestamp":1546300800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2019,1,1]],"date-time":"2019-01-01T00:00:00Z","timestamp":1546300800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cells Tissues Organs"],"published-print":{"date-parts":[[2019]]},"abstract":"<jats:p>The dentate gyrus of the hippocampus is the primary location of adult neurogenesis, which is affected by a variety of external and internal factors, including activity of surrounding glial cells. This study concerns alterations in hippocampal neurogenesis and changes in activity of both proinflammatory and neuroprotective microglia\/macrophages after sciatic nerve injury in the rat. Here, we demonstrated that the chronic pain induced by a peripheral nerve injury manifests in the hippocampus by a decrease in proliferation (PCNA+) and neurogenesis (DCX+), an increase in proinflammatory cytokines (CD86+), and a reduction in neuroprotective (CD163+) microglia\/macrophages. We suggest that a pathological increase microglia\/macrophage activity is the cause of neurogenesis suppression observed in chronic neuropathic pain.<\/jats:p>","DOI":"10.1159\/000501236","type":"journal-article","created":{"date-parts":[[2019,7,8]],"date-time":"2019-07-08T21:00:29Z","timestamp":1562619629000},"page":"58-68","source":"Crossref","is-referenced-by-count":13,"title":["Hippocampal Neurogenesis in Conditions of Chronic Stress Induced by Sciatic Nerve Injury in the 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