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Species | Drug treatment | Experimental approach | Effect on neurogenesis | References |
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Cocaine |
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Cocaine/rat (Sprague-Dawley) | Self-administration (0.5 mg/kg infusion, iv) for 3 weeks. | Proliferation: BrdU (150 mg/kg, ip) once at 2-hours pulsing chase after the last self-administration session. Survival: BrdU at four-week pulsing chase after last self-administration session. | Cell proliferation: decreased number of BrdU+ cells. Survival: no change. | [27] |
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Cocaine/rat (Sprague-Dawley) | 20 mg/kg (ip) for either 1 or 14 days | BrdU once (100 mg/kg, ip) at 2-hour pulsing chase on either 1 or 14 days during cocaine exposure. | One-day cocaine injection: no change in cell proliferation Fourteen-day cocaine injection: decreased cell proliferation | [28, 29] |
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Sprague-Dawley rat | Self-administration (0.5 mg/kg/20 s or 1.5 mg/kg/20 s infusion, iv) for 2 weeks. | Proliferation: BrdU (3 × 50 mg/kg, ip) at 4-hour intervals; analysis twenty-four hours after last BrdU injection. Survival: BrdU (3 × 50 mg/kg, ip) at 4-hour intervals; analysis 4 weeks after last BrdU injection. | Proliferation: decreased number of BrdU+ cells. Survival: decreased neurogenesis. | [30] |
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Cocaine/rat (Wistar) | 20 mg/kg (ip) once daily for 8 days. | BrdU once (40 mg/kg, ip) at 2-hour pulsing chase on final day of cocaine exposure. | Decreased number of BrdU+ cells for cell proliferation. Decreased number of Ki67+ cells with no statistical significance. | [31] |
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Cocaine/rat (Wistar) | 20 mg/kg (ip) daily for 24 days. | BrdU (40 mg/kg, ip) daily for 7 days during the first 7days of cocaine exposure and Ki67 immunostaining. | Decreased number of Ki67+ cells for cell proliferation. No effect on survival. | [31] |
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Cocaine/rat (Wistar) | 20 mg/kg (ip) daily for either 8 or 24 days. | BrdU (2 × 140mg/kg, ip) at 6-hour intervals and 24hours before receiving cocaine exposure. | Both 8-and 24-day cocaine injection: no effect on maturation | [31] |
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Alcohol |
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Sprague-Dawley rat | Acute: EtOH (5 g/kg) by gavage. Chronic: EtOH (5 g/kg) via intragastric catheter on every 8 hours for 4 days. | Proliferation: Acute: BrdU (2 × 100 mg/kg, ip) at 4 hours 15 minutes and 2 hours and 15 minutes pulsing chase. Chronic: BrdU (4 × 100 mg/kg, ip) daily for 4-day binge EtOH Survival: Acute: BrdU (2 × 100 mg/kg, ip) at 4-week pulsing chase. Chronic: BrdU (4 × 50 mg/kg, ip) at 4-week pulsing chase. | Acute: both proliferation and neuronal maturation decreased. Chronic: both proliferation and neuronal maturation decreased. | [32] |
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Sprague-Dawley rat | EtOH (final concentration, 6.4% vol/vol) by gavage for 6 weeks. | Proliferation: BrdU (7 × 40 mg/kg, ip) at 2-hour intervals; animals were sacrificed 1 hour after last BrdU injection. Survival: BrdU (40 mg/kg, ip) once daily for first 10 days of 6 weeks EtOH binge; animals were sacrificed 32 days after the last dose of EtOH. | Proliferation: decreased cell proliferation. Maturation and survival: decreased neuronal maturation. | [33] |
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Wistar rat | Alcohol nondependent: Self-administered alcohol for 3 weeks and exposed air for 10 weeks. Alcohol dependent: Self-administered alcohol for 3 weeks and exposed to intermittent alcohol vapors for 10 weeks. | At week 6, BrdU (150 mg/kg, ip) at 4-week pulsing chase. Immunostaining: Fluoro-Jade C: cell death neuronal degeneration AC-3: apoptotic cells. Ki-67: proliferating cells. DCX: immature neurons. NeuN: mature neurons. | Nondependent drinking: increased cell death and decreased cell proliferation, immature neurons and survival. Dependent drinking: increased cell death and decreased cell proliferation, immature neurons and survival. | [34] |
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C57BL/6J mouse | EtOH by gavage for 28 days and abstinence for either 1 or 14 days. | BrdU (3 × 300 mg/kg, ip) at 4 weeks pulsing chase. Immunostaining: DCX: immature neurons PCNA: proliferating cell marker Behavior tests: open-field locomotor activity and forced swimming test. | Abstinence following alcohol drinking caused: (i) no change in survival of neuronal progenitor cells. (ii) decreased proliferative activity of progenitor cells. (iii) decreased neurogenesis. (iv) increased depressive-like behavior. (v) transiently (1 day abstinence) increased locomotor activity. | [35] |
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Rhesus Monkey | Alcohol induction: EtOH (1%) by gavage for 40 sessions. Alcohol self-administration: EtOH (6%) by gavage for 200 sessions over 11 months. Alcohol abstinence: abstinence for 2–2.5 months. | Immunostaining: Fluoro-Jade C: cell death neuronal degeneration AC-3: apoptotic cells. Ki-67: proliferating cells. GFAP: radial glia-like stem cell and astrocyte marker. SOX2: amplifying neural progenitor cell marker. NeuroD1: immature neurons. PSA-NCAM: mature neurons. | Abstinence following alcohol drinking caused: (i) decreased neurogenesis, (ii) decreased proliferative activity of progenitor cells in initial phases of neuronal development. | [36] |
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