Alcohol and adult hippocampal neurogenesis: Promiscuous drug, wanton effects

Geil, Chelsea R.; Hayes, Dayna M.; McClain, Justin A.; Liput, Daniel J.; Marshall, S. Alex; Chen, Kevin Y.; Nixon, Kimberly

doi:10.1016/j.pnpbp.2014.05.003

Cited by 82 publications

(70 citation statements)

References 225 publications

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“…Furthermore, a preclinical study reported reductions in accumbal volume in alcohol-naïve rats with a genetic predisposition to alcohol addiction (Gozzi et al, 2013), suggesting that accumbal volume reductions may be a pre-existing condition resulting in a vulnerability to alcohol addiction. ADO individuals also had decreased hippocampal volume, which is consistent with the literature on the hippocampal volume and alcohol use disorder (Agartz et al, 1999; Fein and Fein, 2013; Sullivan et al, 1995; Wrase et al, 2008), and corresponds to preclinical findings of hippocampal neurodegeneration due to alcohol exposure (Geil et al, 2014). There was also decreased volume in the right thalamus in both ADO and PS individuals, and decreased left thalamic volume in PS individuals.…”

Section: Discussionsupporting

confidence: 89%

Decreased subcortical volumes in alcohol dependent individuals: effect of polysubstance use disorder

Grodin

Momenan

2016

Addiction Biology

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Chronic alcohol use has widespread effects on brain morphometry. Alcohol dependent individuals are often diagnosed with comorbid substance use disorders. Alterations in brain morphometry may be different in individuals that are dependent on alcohol alone and individuals dependent on alcohol and other substances. We examined subcortical brain volumes in 37 individuals with alcohol dependence only (ADO), 37 individuals with polysubstance use disorder (PS), and 37 healthy control participants (HC). Participants underwent a structural MR scan and a model-based segmentation tool was used to measure the volume of 14 subcortical regions (bilateral thalamus, caudate, putamen, globus pallidus, hippocampus, amygdala, and nucleus accumbens). Compared to HC, ADO had smaller volume in the bilateral hippocampus, right nucleus accumbens, and right thalamus. PS only had volume reductions in the bilateral thalamus compared to HC. PS had a larger right caudate compared to ADO. Subcortical volume was negatively associated with drinking measures only in the ADO group. This study confirms the association between alcohol dependence and reductions in subcortical brain volume. It also suggests that polysubstance use interacts with alcohol use to produce limited subcortical volume reduction and at least one region of subcortical volume increase. These findings indicate that additional substance use may mask damage through inflammation or may function in a protective manner, shielding subcortical regions from alcohol-induced damage.

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Section: Discussionsupporting

confidence: 89%

Decreased subcortical volumes in alcohol dependent individuals: effect of polysubstance use disorder

Grodin

Momenan

2016

Addiction Biology

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“…AIE has been associated with dysfunction in key learning and memory structures in adult rodents. Although AIE leads to decreased neurogenesis within the hippocampus (Geil et al, 2014; Vetreno and Crews, 2015; Sakharkar et al, 2016), AIE’s detrimental effects on spatial memory are inconclusive (Risher et al, 2013; Swartzwelder et al, 2015; Beaudet et al, 2016). Following AIE, there is also a significant loss in the number of cholinergic neurons within the medial septum/diagonal band (MS/DB), which projects to the hippocampus, and the Nucleus basalis of Meynert (NbM) that projects to the cortex (Ehlers et al, 2011; Vetreno et al, 2014; Boutros et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Adolescent binge ethanol exposure alters specific forebrain cholinergic cell populations and leads to selective functional deficits in the prefrontal cortex

Fernandez

Savage

2017

Neuroscience

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Adolescence has been identified as a vulnerable developmental time period during which exposure to drugs can have long-lasting, detrimental effects. Although adolescent binge-like ethanol (EtOH) exposure leads to a significant reduction of forebrain cholinergic neurons, EtOH’s functional effect on acetylcholine (ACh) release during behavior has yet to be examined. Using an adolescent intermittent ethanol exposure model (AIE), rats were exposed to binge-like levels of EtOH from postnatal day (PD) 25–55. Three weeks following the final EtOH exposure, cholinergic functioning was assessed during a spontaneous alternation protocol. During maze testing, ACh levels increased in both the hippocampus and prefrontal cortex. However, selectively in the prefrontal cortex, AIE rats displayed reduced levels of behaviorally-relevant ACh efflux. We found no treatment differences in spatial exploration, spatial learning, spatial reversal, or novel object recognition. In contrast, AIE rats were impaired during the first attentional set shift on an operant set-shifting task, indicative of an EtOH-mediated deficit in cognitive flexibility. A unique pattern of cholinergic cell loss was observed in the basal forebrain following AIE: Within the medial septum/diagonal band there was a selective loss (30%) of choline acetyltransferase (ChAT) positive neurons that were nestin negative (ChAT+/ nestin−); whereas in the Nucleus basalis of Meynert (NbM) there was a selective reduction (50%) in ChAT+/ nestin+. These results indicate that early adolescent binge EtOH exposure leads to a long-lasting frontocortical functional cholinergic deficit, driven by a loss of ChAT+/ nestin+ neurons in the NbM, which was associated with impaired cognitive flexibility during adulthood.

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“…Recent studies indicate that alcohol is involved in the regulation of adult neurogenesis by controlling NSPC proliferation [117, 118]. Alcohol was shown to inhibit NSPC proliferation in adult rats with the paradigms of both acute and chronic binge underlying alcoholic cognitive dysfunction.…”

Section: Modulation Of Nspcs By Addictive Drugs and Underlying Mechanmentioning

confidence: 99%

Effects of addictive drugs on adult neural stem/progenitor cells

Loh

Law

2015

Cell. Mol. Life Sci.

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Neural stem/progenitor cells (NSPCs) undergo a series of developmental processes before giving rise to newborn neurons, astrocytes and oligodendrocytes in adult neurogenesis. During the past decade, the role of NSPCs has been highlighted by studies on adult neurogenesis modulated by addictive drugs. It has been proven that these drugs regulate the proliferation, differentiation and survival of adult NSPCs in different manners, which results in the varying consequences of adult neurogenesis. The effects of addictive drugs on NSPCs are exerted via a variety of different mechanisms and pathways, which interact with one another and contribute to the complexity of NSPC regulation. Here, we review the effects of different addictive drugs on NSPCs, and the related experimental methods and paradigms. We also discuss the current understanding of major signaling molecules, especially the putative common mechanisms, underlying such effects. Finally, we review the future directions of research in this area.

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Alcohol and adult hippocampal neurogenesis: Promiscuous drug, wanton effects

Cited by 82 publications

References 225 publications

Decreased subcortical volumes in alcohol dependent individuals: effect of polysubstance use disorder

Decreased subcortical volumes in alcohol dependent individuals: effect of polysubstance use disorder

Adolescent binge ethanol exposure alters specific forebrain cholinergic cell populations and leads to selective functional deficits in the prefrontal cortex

Effects of addictive drugs on adult neural stem/progenitor cells

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