Chronic Intermittent Ethanol Exposure Increases Ethanol Consumption Following Traumatic Stress Exposure in Mice

Piggott, Veronica M; Lloyd, Scott C; Perrine, Shane A.; Conti, Alana C.

doi:10.3389/fnbeh.2020.00114

Cited by 7 publications

(5 citation statements)

References 62 publications

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“…This hyperlocomotion was accompanied by hyperactivity as evidenced by increased average speed in center of the open-field apparatus ( Figure 2D , p = 0.0008, t -test), total average speed ( Figure 2E , p < 0.0001, t -test) in the OF apparatus, and reduced latency to feed in the NSF, compared to water controls ( Figure 2F , p = 0.0005, t -test). Combined with hyperactivity, this lack of novelty-induced feeding inhibition could be interpreted as a reduction of impulse control to anxiogenic environment and further suggests that chronic sucrose consumption produces both hyperactivity and impulsivity ( Bevilacqua et al, 2010 ; Angoa-Pérez et al, 2014 ; Piggott et al, 2020 ).…”

Section: Resultsmentioning

confidence: 99%

“…Interestingly, long-term sucrose consumption reduced impulse control in the novelty-suppressed feeding, and this was not observed when sucrose access was restricted. Although novelty-suppressed feeding test is primarily to assess anxiety-like behaviors, studies have shown that a reduced latency to feed could be correlated with augmented food seeking and increased meal size ( Biddinger et al, 2020 ), increased hunger and reduced-feeding control after fasting ( Burghardt et al, 2016 ), and together with hyperlocomotion, increased motor impulsivity ( Bevilacqua et al, 2010 ; Angoa-Pérez et al, 2014 ; Piggott et al, 2020 ). This suggests that the reduced latency to feed we observed after long-term sucrose intake could be the result of impulsivity.…”

Section: Discussionmentioning

confidence: 99%

“…To understand how sucrose overconsumption affects hyperactivity and compulsion, we assessed general locomotor activity using OF. To evaluate impulse control we used the NSF, conflict based anxiety test that has previously been shown to reflect impulsivity-like behavior (Bevilacqua et al, 2010;Angoa-Pérez et al, 2014;Piggott et al, 2020). Sucrose consuming mice displayed a higher general locomotor activity as observed by an increase in total distance traveled (Figures 2B,C) compared to water control animals (Figures 2A,C, p < 0.0001, t-test).…”

Section: Long-term Sucrose Intake Produces Hyperactivity/hyperlocomotionmentioning

confidence: 99%

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Long-Term Overconsumption of Sugar Starting at Adolescence Produces Persistent Hyperactivity and Neurocognitive Deficits in Adulthood

et al. 2021

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Sugar has become embedded in modern food and beverages. This has led to overconsumption of sugar in children, adolescents, and adults, with more than 60 countries consuming more than four times (>100 g/person/day) the WHO recommendations (25 g/person/day). Recent evidence suggests that obesity and impulsivity from poor dietary habits leads to further overconsumption of processed food and beverages. The long-term effects on cognitive processes and hyperactivity from sugar overconsumption, beginning at adolescence are not known. Using a well-validated mouse model of sugar consumption, we found that long-term sugar consumption, at a level that significantly augments weight gain, elicits an abnormal hyperlocomotor response to novelty and alters both episodic and spatial memory. Our results are similar to those reported in attention deficit and hyperactivity disorders. The deficits in hippocampal-dependent learning and memory were accompanied by altered hippocampal neurogenesis, with an overall decrease in the proliferation and differentiation of newborn neurons within the dentate gyrus. This suggests that long-term overconsumption of sugar, as that which occurs in the Western Diet might contribute to an increased risk of developing persistent hyperactivity and neurocognitive deficits in adulthood.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Long-term Sucrose Intake Produces Hyperactivity/hyperlocomotionmentioning

confidence: 99%

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Long-Term Overconsumption of Sugar Starting at Adolescence Produces Persistent Hyperactivity and Neurocognitive Deficits in Adulthood

et al. 2021

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“…While some work has exposed animals to EtOH prior to PTSD‐like stressors, these experiments assess changes in EtOH drinking following stress and do not examine EtOH‐induced changes in PTSD‐like behavior itself. For example, previous exposure to EtOH increases EtOH preference and consumption following exposure to PTSD‐like stressors (Piggott et al, 2020). Likewise, Zoladz et al (2018) confirmed that PTSD‐like stress increases EtOH intake in EtOH‐experienced animals, but also demonstrated that stress leads to decreased EtOH intake in EtOH‐naïve animals.…”

Section: Introductionmentioning

confidence: 99%

Chronic ethanol consumption exacerbates future stress‐enhanced fear learning, an effect mediated by dorsal hippocampal astrocytes

Barkell

Parekh

Paniccia

et al. 2022

Alcoholism Clin & Exp Res

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Background: Alcohol use disorder (AUD) and post-traumatic stress disorder (PTSD) are highly comorbid, yet there is a lack of preclinical research investigating how prior ethanol (EtOH) dependence influences the development of a PTSD-like phenotype.Furthermore, the neuroimmune system has been implicated in the development of both AUD and PTSD, but the extent of glial involvement in this context remains unclear. A rodent model was developed to address this gap in the literature. Methods:We used a 15-day exposure to the 5% w/v EtOH low-fat Lieber-DeCarli liquid diet in combination with the stress-enhanced fear learning (SEFL) paradigm to investigate the effects of chronic EtOH consumption on the development of a PTSDlike phenotype. Next, we used a reverse transcription quantitative real-time polymerase chain reaction to quantify mRNA expression of glial cell markers GFAP (astrocytes) and CD68 (microglia) following severe footshock stress in EtOH-withdrawn rats.Finally, we tested the functional contribution of dorsal hippocampal (DH) astrocytes in the development of SEFL in EtOH-dependent rats using astrocyte-specific G i designer receptors exclusively activated by designer drugs (G i -DREADD).Results: Results demonstrate that chronic EtOH consumption and withdrawal exacerbate future SEFL. Additionally, we found significantly increased GFAP mRNA expression in the dorsal and ventral hippocampus and amygdalar complex following the severe stressor in EtOH-withdrawn animals. Finally, the stimulation of the astroglial G i -DREADD during EtOH withdrawal prevented the EtOH-induced enhancement of SEFL. Conclusions: Collectively, results indicate that prior EtOH dependence and withdrawal combined with a severe stressor potentiate future enhanced fear learning. Furthermore, DH astrocytes significantly contribute to this change in behavior. Overall, these studies provide insight into the comorbidity of AUD and PTSD and the potential neurobiological mechanisms behind increased susceptibility to a PTSD-like phenotype in individuals with AUD.

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“…Our previous study showed that traumatic stress combined with acute alcohol administration decreased CB1R levels in the mouse anterior STR compared to control groups [ 20 ]. Our previous reports have also shown that traumatic stress combined with chronic intermittent ethanol vapor exposure and withdrawal uniquely increased ethanol consumption compared to the control group (non-stress, air exposure) in mice [ 57 ]. However, no animal studies have been reported to examine the effects of traumatic stress combined with chronic ethanol exposure on the brain levels of the endocannabinoid ligands (AEA and 2-AG), their synthetic enzymes (NAPE-PLD and α-DAGL), their degradatory-hydrolytic enzymes (FAAH and MAG-L), and CB1R.…”

Section: Introductionmentioning

confidence: 99%

Traumatic Stress, Chronic Ethanol Exposure, or the Combination, Alter Cannabinoid System Components in Reward and Limbic Regions of the Mouse Brain

et al. 2021

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The cannabinoid system is independently affected by stress and chronic ethanol exposure. However, the extent to which co-occurrence of traumatic stress and chronic ethanol exposure modulates the cannabinoid system remains unclear. We examined levels of cannabinoid system components, anandamide, 2-arachidonoylglycerol, fatty acid amide hydrolase, and monoacylglycerol lipase after mouse single-prolonged stress (mSPS) or non-mSPS (Control) exposure, with chronic intermittent ethanol (CIE) vapor or without CIE vapor (Air) across several brain regions using ultra-high-performance liquid chromatography tandem mass spectrometry or immunoblotting. Compared to mSPS-Air mice, anandamide and 2-arachidonoylglycerol levels in the anterior striatum were increased in mSPS-CIE mice. In the dorsal hippocampus, anandamide content was increased in Control-CIE mice compared to Control-Air, mSPS-Air, or mSPS-CIE mice. Finally, amygdalar anandamide content was increased in Control-CIE mice compared to Control-Air, or mSPS-CIE mice, but the anandamide content was decreased in mSPS-CIE compared to mSPS-Air mice. Based on these data we conclude that the effects of combined traumatic stress and chronic ethanol exposure on the cannabinoid system in reward pathway regions are driven by CIE exposure and that traumatic stress affects the cannabinoid components in limbic regions, warranting future investigation of neurotherapeutic treatment to attenuate these effects.

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Chronic Intermittent Ethanol Exposure Increases Ethanol Consumption Following Traumatic Stress Exposure in Mice

Cited by 7 publications

References 62 publications

Long-Term Overconsumption of Sugar Starting at Adolescence Produces Persistent Hyperactivity and Neurocognitive Deficits in Adulthood

Long-Term Overconsumption of Sugar Starting at Adolescence Produces Persistent Hyperactivity and Neurocognitive Deficits in Adulthood

Chronic ethanol consumption exacerbates future stress‐enhanced fear learning, an effect mediated by dorsal hippocampal astrocytes

Traumatic Stress, Chronic Ethanol Exposure, or the Combination, Alter Cannabinoid System Components in Reward and Limbic Regions of the Mouse Brain

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