The neural, behavioral, and epidemiological underpinnings of comorbid alcohol use disorder and post-traumatic stress disorder

Carlson, Hannah N.; Weiner, Jeff L.

doi:10.1016/bs.irn.2020.09.006

Cited by 14 publications

(14 citation statements)

References 282 publications

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“…Epidemiological evidence of co-occurring PTSD and AUD spans decades and continents, revealing the vast global impact of these disorders with one another (Helzer et al, 1987;Bremner et al, 1996;Mills et al, 2006;Kachadourian & Petrakis, 2016;Smith & Cottler, 2018). Dual-diagnosed individuals with PTSD and AUD experience increased negative affective mood and behaviors, as each disorder acts as a risk factor for the other (Carlson & Weiner, 2021). Markedly, research has shown that treatment options for individuals with a dualdiagnosis are less effective and have poorer outcomes compared to treating individuals diagnosed with either PTSD or AUD alone (McCauley et al, 2012).…”

Section: Main Textmentioning

confidence: 99%

Hippocampal fear engrams modulate ethanol-induced maladaptive contextual generalization in mice

Cincotta

Ruesch

Senne

et al. 2022

Preprint

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The compounding symptomatology of comorbid alcohol use disorder (AUD) and post-traumatic stress disorder (PTSD) gives rise to an interaction of maladaptive neurobiological processes, the etiology of which remains elusive. Here, we devised an optogenetic strategy aimed at rescuing maladaptive responses to fearful stimuli in male c57BL/6 mice following chronic ethanol administration and forced abstinence. In the first experiment, we confirmed that fear acquisition and maladaptive contextual generalization was potentiated in ethanol-exposed mice during fear conditioning and exposure to a novel environment, respectively. In the second experiment, using an activity-dependent tet-tag system, we labeled and artificially inhibited the neural ensemble selectively activated by contextual fear conditioning in the dorsal hippocampus to attenuate behavioral dysfunctions resulting from ethanol exposure. We found that acute optogenetic inhibition during exposure to a novel environment suppressed maladaptive generalization in ethanol-exposed mice. These results provide further evidence for a crucial link between ethanol exposure and impaired fear memory processing by providing cellular and behavioral insights into the neural circuitry underlying AUD and PTSD comorbidity.

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Section: Main Textmentioning

confidence: 99%

Hippocampal fear engrams modulate ethanol-induced maladaptive contextual generalization in mice

Cincotta

Ruesch

Senne

et al. 2022

Preprint

View full text Add to dashboard Cite

show abstract

“…Beyond substance use serving as a risk factor for later traumatic event exposure, another example stems from recent epidemiological studies positing that PTSD often develops prior to problematic substance use [ 16 ]. Specifically, the “self-medication hypothesis” [ 17 ] is a negative reinforcement etiologic model that suggests when youth experience trauma-related distress, the youth is primarily motivated to engage in strategies, such as substance use, to avoid or decrease the distress and negative affective state.…”

Section: Overlapping Clinical Symptomatologymentioning

confidence: 99%

Elucidating the Neurobiologic Etiology of Comorbid PTSD and Substance Use Disorders

Hinckley

Danielson

2022

Brain Sciences

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Early childhood maltreatment and other traumatic event experiences (“trauma”) are common among youth, including those with substance use problems including substance use disorders (SUD). Particularly, interpersonal violence is associated with high rates of comorbidity between posttraumatic stress disorder (PTSD) and SUD, and these comorbid disorders exhibit high levels of overlapping symptomatology. Theoretical models proposed to explain the bidirectional relationship between PTSD and SUD include the self-medication hypothesis and susceptibility hypothesis. In this article, we explore neurobiologic changes associated with trauma, PTSD, and SUD that underly dysregulated stress response. Examining lessons learned from recent translational and clinical research, we propose that further elucidating the neurobiologic etiology of comorbid PTSD and SUD will require a collaborative, interdisciplinary approach, including the integration of preclinical and clinical studies, exploration of biologic markers in clinical studies, and accumulation of larger studies and longitudinal studies with the power to study PTSD and SUD. Such research can transform the field and ultimately reduce high rates and costly impairment of co-occurring PTSD and SUD across the lifespan.

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“…In particular, symptoms of psychiatric disorders in which aberrant fear responses are a core component, including but not limited to post traumatic stress disorder (PTSD) and generalized anxiety, are often intensified by drug and alcohol use (Anker & Kushner, 2019; Neupane et al, 2017). For example, dual‐diagnosed individuals with PTSD and AUD experience increased negative affective mood and behaviors, as each disorder acts as a risk factor for the other (Carlson & Weiner, 2021). Markedly, research has shown that treatment options for individuals with a dual‐diagnosis are less effective and have poorer outcomes compared to treating individuals diagnosed with either PTSD or AUD alone (McCauley et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Hippocampal fear engrams modulate ethanol‐induced maladaptive contextual generalization in mice

et al. 2022

View full text Add to dashboard Cite

The compounding symptomatology of alcohol use disorder (AUD) and co‐occurring mental health disorders gives rise to interactions of maladaptive neurobiological processes, the etiology of which are elusive. Here, we devised an optogenetic strategy aimed at rescuing maladaptive fear processing in male c57BL/6 mice that underwent a chronic ethanol administration and forced abstinence paradigm. In the first experiment, we confirmed that fear acquisition and maladaptive contextual generalization was potentiated in ethanol‐exposed mice during fear conditioning and exposure to a novel environment, respectively. In the second experiment, using an activity‐dependent tet‐tag system, we labeled the neural ensemble selectively activated by contextual fear conditioning in the dorsal hippocampus with an inhibitory opsin to attenuate behavioral dysfunctions resulting from ethanol exposure. We found that acute optogenetic perturbations during exposure to a novel environment suppressed maladaptive generalization in ethanol‐exposed mice. These results provide further evidence for a crucial link between ethanol exposure and impaired fear memory processing by providing cellular and behavioral insights into the neural circuitry underlying AUD and maladaptive fear processing.

show abstract

The neural, behavioral, and epidemiological underpinnings of comorbid alcohol use disorder and post-traumatic stress disorder

Cited by 14 publications

References 282 publications

Hippocampal fear engrams modulate ethanol-induced maladaptive contextual generalization in mice

Hippocampal fear engrams modulate ethanol-induced maladaptive contextual generalization in mice

Elucidating the Neurobiologic Etiology of Comorbid PTSD and Substance Use Disorders

Hippocampal fear engrams modulate ethanol‐induced maladaptive contextual generalization in mice

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