Archival ReportDrug-Dependent Requirement of Hippocampal Neurogenesis in a Model of Depression and of Antidepressant Reversal
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Animals
Two-month-old male BALB/c mice were obtained from Taconic (Germantown, New York). All animals were housed in groups of four or five and were maintained under standard laboratory conditions (12/12-hour light/dark cycle: lights on at 8:00 pm, 22 ± 2°C, food and water ad libitum). The treatment of the animals was in accordance with the European Community Council directive 86/609/EEC and with the Guide for Care and Use of Laboratory Animals established by the National Institutes of Health of the
Disruption of Hippocampal Neurogenesis Has No Effect on Sensitivity to Stress
To determine whether loss of neurogenesis alters sensitivity to stress, we compared the responses of irradiated and non-irradiated mice to UCMS. In vehicle-treated mice, UCMS induced a gradual deterioration of coat state that reached significance by 4 weeks after beginning the stress (p < .001) and worsened until the end of the stress procedure (p < .001; Figure 2A). This effect was accompanied by reduced grooming in the splash test (p < .01; Figure 2B) and increased latency to eat in the NSF
Discussion
The UCMS-induced behavioral changes were reversed by several compounds endowed with AD-like properties, such as fluoxetine and imipramine, as well as a CRF1 antagonist (SSR125543) and a V1b antagonist (SSR149415). The x-irradiation of the hippocampus had no effect per se in the UCMS procedure, suggesting that a loss of hippocampal neurogenesis does not induce a depressive-like behavior and does not worsen the deteriorations induced by the UCMS. Nevertheless, irradiation completely abolished the
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