Literature DB >> 18585922

Distinct cell proliferation events during abstinence after alcohol dependence: microglia proliferation precedes neurogenesis.

K Nixon1, D H Kim, E N Potts, J He, F T Crews.   

Abstract

Excessive alcohol intake characteristic of Alcohol Use Disorders (AUDs) produces neurodegeneration that may recover with abstinence. The mechanism of regeneration is unclear, however neurogenesis from neural stem/progenitor cells is a feasible mechanism of structural plasticity. Therefore, a timecourse of cell proliferation was examined in a rat model of an AUD and showed a striking burst in cell proliferation at 2 days of abstinence preceding the previously reported neurogenic proliferation at 7 days. New cells at 2 days, assessed by bromo-deoxy-uridine incorporation and endogenous markers, were observed throughout hippocampus and cortex. Although the majority of these new cells did not become neurons, neurogenesis was not altered at this specific time point. These new cells expressed a microglia-specific marker, Iba-1, and survived at least 2 months. This first report of microglia proliferation in a model of an AUD suggests that microgliosis could contribute to volume recovery in non-neurogenic regions during abstinence.

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Year:  2008        PMID: 18585922      PMCID: PMC2680247          DOI: 10.1016/j.nbd.2008.04.009

Source DB:  PubMed          Journal:  Neurobiol Dis        ISSN: 0969-9961            Impact factor:   5.996


  78 in total

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  58 in total

1.  Upregulated vimentin suggests new areas of neurodegeneration in a model of an alcohol use disorder.

Authors:  M L Kelso; D J Liput; D W Eaves; K Nixon
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Review 2.  Glial abnormalities in substance use disorders and depression: does shared glutamatergic dysfunction contribute to comorbidity?

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6.  Hippocampal neural progenitor cells play a distinct role in fear memory retrieval in male and female CIE rats.

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7.  Alcohol dependence-induced regulation of the proliferation and survival of adult brain progenitors is associated with altered BDNF-TrkB signaling.

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8.  Persistent loss of hippocampal neurogenesis and increased cell death following adolescent, but not adult, chronic ethanol exposure.

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Review 9.  Cognitive Decline and Recovery in Alcohol Abuse.

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10.  Activation of neural stem cells from quiescence drives reactive hippocampal neurogenesis after alcohol dependence.

Authors:  Dayna M Hayes; Chelsea G Nickell; Kevin Y Chen; Justin A McClain; Megan M Heath; M Ayumi Deeny; Kimberly Nixon
Journal:  Neuropharmacology       Date:  2018-01-31       Impact factor: 5.250

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