Thinking after Drinking: Impaired Hippocampal-Dependent Cognition in Human Alcoholics and Animal Models of Alcohol Dependence

Staples, Miranda C.; Mandyam, Chitra D.

doi:10.3389/fpsyt.2016.00162

Cited by 30 publications

(28 citation statements)

References 171 publications

(157 reference statements)

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“…New emerging evidence has suggested that altered neurogenesis and gliogenesis may contribute to drug taking and drug seeking (Mandyam and Koob, 2012 ). Further, studies suggest that drug-induced loss of neurogenesis contributes to addiction and recovery from a variety of drugs, including alcohol (Mandyam and Koob, 2012 ; Staples and Mandyam, 2016 ). Previous studies have found that chronic ethanol treatment of adult rats reduces NPC proliferation in the DG (Nixon and Crews, 2002 ; Herrera et al, 2003 ; He et al, 2005 ) and SVZ (Crews et al, 2004 ; Hansson et al, 2010 ; Campbell et al, 2014 ).…”

Section: Introductionmentioning

confidence: 99%

Persistent Decreases in Adult Subventricular and Hippocampal Neurogenesis Following Adolescent Intermittent Ethanol Exposure

Crews

2017

Front. Behav. Neurosci.

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Neurogenesis in hippocampal dentate gyrus (DG) and subventricular zone (SVZ) matures during adolescence to adult levels. Binge drinking is prevalent in adolescent humans, and could alter brain neurogenesis and maturation in a manner that persists into adulthood. To determine the impact of adolescent binge drinking on adult neurogenesis, Wistar rats received adolescent intermittent ethanol (AIE) exposure (5.0 g/kg/day, i.g., 2 days on/2 days off from postnatal day, P25–P54) and sacrificed on P57 or P95. Neural progenitor cell proliferation, differentiation, survival and maturation using immunohistochemistry was determined in the DG and SVZ. We found that AIE exposure decreased neurogenesis in both brain regions in adulthood (P95). In the DG at P57, AIE exposure resulted in a significant reduction of SOX2+, Tbr2+, Prox1+ and parvalbumin (PV)+IR expression, and at P95 decreased DCX+ and PV+IR expression. AIE exposure also reduced the expression of two cell proliferation markers (Ki67+ and BrdU+IR with 300 mg/kg, 2 h) at P95. The immune signaling molecule β-2 microglobulin+ and the cell death marker activated caspase-3+IR were significantly increased in the DG by AIE exposure. In the SVZ, AIE exposure decreased SOX2+, Mash1+, DCX+ and Dlx2+IR expression at P95, but not at P57. Thus, in adulthood both brain regions have reduced neurogenesis following AIE exposure. To assess progenitor cell survival and maturation, rats were treated with BrdU (150 mg/kg/day, 14 days) to label proliferating cells and were sacrificed weeks later on P95. In the hippocampus DG, AIE exposure increased survival BrdU+ cells which differentiated into Iba1+ microglia. In contrast, SVZ had decreased BrdU+ cells similar to decreased DCX+ neurogenesis. These data indicate that AIE exposure causes a lasting decrease in both adult hippocampal DG and forebrain SVZ neurogenesis with brain regional differences in the AIE response that persist into adulthood.

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Section: Introductionmentioning

confidence: 99%

Persistent Decreases in Adult Subventricular and Hippocampal Neurogenesis Following Adolescent Intermittent Ethanol Exposure

Crews

2017

Front. Behav. Neurosci.

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“…Indeed, some studies have revealed decreases in hippocampal volume in AUD patients, although these changes have been shown to revert with abstinence (reviewed in [61]). There is also evidence of impairment in hippocampus-related functions as consequence of problematic alcohol consumption, effects that, similarly to those found in volumetric studies, could improve with abstinence [62].…”

Section: Clinical Evidence Of Auds Contributing To Hippocampal Neurogmentioning

confidence: 56%

“…In this regard, clinical studies found that deficits in hippocampal volume in AUD patients compared with healthy controls normalize over an abstinence period of 2 weeks [83] and that hippocampal volume did not constitute a predictive factor for relapse risk in abstinent alcoholics [84]. On the other hand, it has been observed that the hippocampal-dependent functions could continue to be altered even in prolonged abstinence [62], which could be a factor that, as other authors propose,…”

Section: Clinical Evidence Of Hippocampal Neurogenesis Deterioration mentioning

confidence: 99%

Rethinking the Use of Antidepressants to Treat Alcohol Use Disorders and Depression Comorbidity: The Role of Neurogenesis

Ballesta¹,

Alén²,

Fonseca³

et al. 2019

Antidepressants - Preclinical, Clinical and Translational Aspects

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Patients with alcohol use disorders (AUDs) are frequently treated with antidepressant drugs (ADs), but clinical evidence of their efficacy is contradictory. Considering that ADs are thought to produce their therapeutic effects partially by increasing hippocampal plasticity and neurogenesis (HN), and that both AUDs and depression share a potential for the disruption of these neuroplastic processes, one could reasonably wonder whether the poor efficacy of AD treatment could be explained by the inability of these drugs to exert their proper action in patients suffering from AUD or depression. In order to further clarify this question, this chapter aims to examine available data regarding the effect of ADs on behavioral and HN alterations related to alcohol abstinence, as a key period in which the treatment would be implemented and in which their potential effects on alcohol-related problems remain under controversy.

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“…Magnetic resonance imaging (MRI) has been used extensively to study morphological changes in the brain associated with alcohol use disorder (AUD), a widespread and harmful condition [1,2] . Because memory impairments are associated with long-term chronic AUD, one neuroanatomical focus of investigation has been the hippocampus [3] . Moreover, findings from previous research have shown that the largest subcortical volume loss observed in the brains of people with chronic AUD was in the hippocampus [4] , and a meta-analysis [5] found a negative association between total hippocampal volume and degree of alcohol use (clinical vs. subclinical).…”

Section: Introductionmentioning

confidence: 99%

Hippocampal Subfield Volumes in Abstinent Men and Women with a History of Alcohol Use Disorder

Sawyer

Salz

Adra

et al. 2019

Preprint

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Alcohol use disorder (AUD) has been associated with abnormalities in hippocampal volumes, but these relationships have not been fully explored with respect to sub-regional volumes, nor in association with individual characteristics such as gender differences, age, and memory. The present study examined the impact of those variables in relation to hippocampal subfield volumes in abstinent men and women with a history of AUD. Using Magnetic Resonance Imaging at 3 Tesla, we obtained brain images from 67 participants (31 women) with AUD and 63 healthy control (NC) participants (30 women) without AUD. We used Freesurfer 6.0 to segment the hippocampus into 12 regions. These were imputed into mixed models to examine the relationships of brain volume with AUD group, gender, age, drinking history, and memory.The AUD group had approximately 5% smaller CA1, hippocampal tail, and molecular layer regions than the NC group. Age was negatively associated with volumes for the AUD group in the hippocampal tail, subiculum, and presubiculum. The relationships for delayed and immediate memory with hippocampal tail volume differed for AUD and NC groups: Higher scores were associated with smaller volumes in the AUD group, but larger volumes in the NC group. Length of sobriety was associated with decreasing CA1 volume in women (0.02% per year) and increasing volume size in men (0.03% per year). These findings confirm and extend evidence that AUD, gender, age, and abstinence differentially impact volumes of component parts of the hippocampus. The course of abstinence on CA1 volume differed for men and women, and the differential relationships of subregional volumes to age and memory could indicate a distinction in the impact of AUD on functions of the hippocampal tail.

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Thinking after Drinking: Impaired Hippocampal-Dependent Cognition in Human Alcoholics and Animal Models of Alcohol Dependence

Cited by 30 publications

References 171 publications

Persistent Decreases in Adult Subventricular and Hippocampal Neurogenesis Following Adolescent Intermittent Ethanol Exposure

Persistent Decreases in Adult Subventricular and Hippocampal Neurogenesis Following Adolescent Intermittent Ethanol Exposure

Rethinking the Use of Antidepressants to Treat Alcohol Use Disorders and Depression Comorbidity: The Role of Neurogenesis

Hippocampal Subfield Volumes in Abstinent Men and Women with a History of Alcohol Use Disorder

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