Permanent impairment of birth and survival of cortical and hippocampal proliferating cells following excessive drinking during alcohol dependence.
paper
Cited
Public
- Authors
- Richardson, Heather N; Chan, Stephanie H; Crawford, Elena F; Lee, Youn Kyung; Funk, Cindy K; Koob, George F; Mandyam, Chitra D
- Year
- 2009
- Journal
- Neurobiology of disease
- PMID
- 19501165
- DOI
- 10.1016/j.nbd.2009.05.021
- PMCID
- PMC2742572
Experimenter-delivered alcohol decreases adult hippocampal neurogenesis and hippocampal-dependent learning and memory. The present study used clinically relevant rodent models of nondependent limited access alcohol self-administration and excessive drinking during alcohol dependence (alcohol self-administration followed by intermittent exposure to alcohol vapors over several weeks) to compare alcohol-induced effects on cortical gliogenesis and hippocampal neurogenesis. Alcohol dependence, but not nondependent drinking, reduced proliferation and survival in the medial prefrontal cortex (mPFC). Apoptosis was reduced in both alcohol groups within the mPFC, which may reflect an initiation of a reparative environment following alcohol exposure as decreased proliferation was abolished after prolonged dependence. Reduced proliferation, differentiation, and neurogenesis were observed in the hippocampus of both alcohol groups, and prolonged dependence worsened the effects. Increased hippocampal apoptosis and neuronal degeneration following alcohol exposure suggest a loss in neuronal turnover and indicate that the hippocampal neurogenic niche is highly vulnerable to alcohol.
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| 20 | Materials and methods β Microscopic analysis and quantification | Cells in the mPFC (i.e., Ki-67-, AC-3-, and BrdU-immunoreactive [IR] cells in the cingulate,β¦ |
| 21 | Materials and methods β Microscopic analysis and quantification | Detailed quantification was performed for DCX-IR cells. DCX is a marker for young neurons, and theβ¦ |
| 22 | Materials and methods β Microscopic analysis and quantification | For BrdU phenotype analysis, every 27th section through the hippocampus was triple-labeled with BrdUβ¦ |
| 23 | Materials and methods β Fluoro-Jade C (FJC) staining | FJC staining was performed as previously described (Schmued et al., 2005). Every 18th sectionβ¦ |
| 24 | Materials and methods β Measurement of hippocampal granule cell number | Quantitative analysis to obtain unbiased estimates of the total number of granule cells wasβ¦ |
| 25 | Materials and methods β Measurement of hippocampal granule cell number | section thickness 21 ΞΌm) through the dentate gyrus of the hippocampus counterstained with Nuclearβ¦ |
| 26 | Materials and methods β Data analysis | Alcohol self-administration data and Ki-67, DCX, AC-3, BrdU and FJC data comparing nondependentβ¦ |
| 27 | Results β Alcohol self-administration behavior: nondependent alcohol self-administration and excessive alcohol self-administration during alcohol dependence (termed henceforth as nondependent drinking and alcohol dependence) | The experimental timeline of operant training, dependence induction, BrdU injection, and perfusionβ¦ |
| 28 | Results β Alcohol self-administration behavior: nondependent alcohol self-administration and excessive alcohol self-administration during alcohol dependence (termed henceforth as nondependent drinking and alcohol dependence) | elicited increased alcohol self-administration in both groups of alcohol-dependent animals comparedβ¦ |
| 29 | Results β Alcohol self-administration behavior: nondependent alcohol self-administration and excessive alcohol self-administration during alcohol dependence (termed henceforth as nondependent drinking and alcohol dependence) | reliable blood alcohol levels: (dependent: (Set I: 193.2 Β± 17.7 mg%; Set II: 159.7 Β± 9.7 mg%; p =β¦ |
| 30 | Results β Alcohol dependence alters apoptosis, proliferation and survival in the mPFC | Sections comprising mPFC from the naive, naive-trained, nondependent and alcohol-dependent animalsβ¦ |
| 31 | Results β Alcohol dependence alters apoptosis, proliferation and survival in the mPFC | solution fading procedure did not alter proliferation. Nondependent drinking did not produce aβ¦ |
| 32 | Results β Nondependent drinking and alcohol dependence alter cell death, proliferation, immature neurons, survival and neurogenesis in the hippocampal SGZ | Hippocampal sections from naive, naive-trained, nondependent and alcohol dependent animals (Set I,β¦ |
| 33 | Results β Nondependent drinking and alcohol dependence alter cell death, proliferation, immature neurons, survival and neurogenesis in the hippocampal SGZ | Cell death was analyzed by probing for two markers, AC-3 to measure apoptotic cell death andβ¦ |
| 34 | Results β Nondependent drinking and alcohol dependence alter cell death, proliferation, immature neurons, survival and neurogenesis in the hippocampal SGZ | Nondependent drinking and alcohol dependence significantly altered SGZ cell proliferation (effect ofβ¦ |
| 35 | Results β Nondependent drinking and alcohol dependence alter cell death, proliferation, immature neurons, survival and neurogenesis in the hippocampal SGZ | Both nondependent and dependent groups show significant reductions in BrdU cell number (survival,β¦ |
| 36 | Results β Prolonged exposure to nondependent and alcohol dependent environment differentially alters proliferation, immature neurons and granule cell neurons in the hippocampal SGZ | Sections from naive, prolonged nondependent, and prolonged dependent animals (Set II, brain tissueβ¦ |
| 37 | Results β Prolonged exposure to nondependent and alcohol dependent environment differentially alters proliferation, immature neurons and granule cell neurons in the hippocampal SGZ | alcohol. On the other hand, prolonged dependence showed a greater decrease in total DCX-IR cellsβ¦ |
| 38 | Discussion | Animal models of nondependent drinking and excessive drinking during alcohol dependence are useful⦠|
| 39 | Discussion | The effects of alcohol on proliferation of cortical precursors has been studied in vitro, in which⦠|
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