Influence of stress associated with chronic alcohol exposure on drinking

Abstract

Stress is commonly regarded as an important trigger for relapse and a significant factor that promotes increased motivation to drink in some individuals. However, the relationship between stress and alcohol is complex, likely changing in form during the transition from early moderated alcohol use to more heavy uncontrolled alcohol intake. A growing body of evidence indicates that prolonged excessive alcohol consumption serves as a potent stressor, producing persistent dysregulation of brain reward and stress systems beyond normal homeostatic limits. This progressive dysfunctional (allostatic) state is characterized by changes in neuroendocrine and brain stress pathways that underlie expression of withdrawal symptoms that reflect a negative affective state (dysphoria, anxiety), as well as increased motivation to self-administer alcohol. This review highlights literature supportive of this theoretical framework for alcohol addiction. In particular, evidence for stress-related neural, physiological, and behavioral changes associated with chronic alcohol exposure and withdrawal experience is presented. Additionally, this review focuses on the effects of chronic alcohol-induced changes in several pro-stress neuropeptides (corticotropin-releasing factor, dynorphin) and anti-stress neuropeptide systems (nocicepton, neuropeptide Y, oxytocin) in contributing to the stress, negative emotional, and motivational consequences of chronic alcohol exposure. Studies involving use of animal models have significantly increased our understanding of the dynamic stress-related physiological mechanisms and psychological underpinnings of alcohol addiction. This, in turn, is crucial for developing new and more effective therapeutics for treating excessive, harmful drinking, particularly stress-enhanced alcohol consumption.

Indicators of Red Blood and T-Lymphocytes in Patients With Alcoholism; Protective Potential of Lithium Ascorbate

“…Напротив, относительное количество зрелых Т-лимфоцитов в 1 точке обследова-ния было повышено по отношению к кон-тролю, что может быть обусловлено вклю-чением компенсаторных механизмов при стрессе, поскольку длительное потребление алкоголя и его отмена является мощным стрессором [13,14]. Проведены предварительные экспери-менты по влиянию аскорбата лития на экс-прессию поверхностных рецепторов лим-фоцитов больных алкоголизмом.…”

Chronic intermittent ethanol exposure selectively increases synaptic excitability in the ventral domain of the rat hippocampus

“…Despite the clinical importance of understanding the neural substrates responsible for the negative affective state that develops following chronic alcohol exposure and withdrawal, much remains unknown regarding the specific brain regions and circuits that mediate withdrawal-associated increases in anxiety behaviors and alcohol drinking. One preclinical model of AUD that has been extensively validated to address these questions is the chronic intermittent ethanol (CIE) vapor exposure regimen (Becker, 2017;Gilpin et al, 2008;Reynolds and Berridge, n.d.;Vendruscolo and Roberts, 2014). Using this model, which involves daily cycles of ethanol vapor exposure followed by a withdrawal period, rats and mice develop physiological and behavioral signs of ethanol dependence, including marked escalations in ethanol self-administration (Criado and Ehlers, 2013;Finn et al, 2007;O'Dell et al, 2004) and increases in anxiety-like behaviors on assays like the elevated plus-maze (Cagetti et al, 2004).…”

The CRF-R1 regulation of VTA-GABAergic plasticity is suppressed by CB1 receptor inhibition following chronic exposure to ethanol

“…The transition from moderate controlled drinking (<2 drinks per day) to heavy drinking (>5 drinks per day) often involves intermittent bouts of binge consumption of ethanol, culminating in dependence (Becker, 2017). Acute administration of ethanol increases the release of mesolimbic dopamine in VTA projection areas (Di Chiara and Imperato, 1988; Yim et al , 1998; Zapata and Shippenberg, 2006).…”

“…Acute administration of ethanol increases the release of mesolimbic dopamine in VTA projection areas (Di Chiara and Imperato, 1988; Yim et al , 1998; Zapata and Shippenberg, 2006). Prolonged excessive alcohol consumption is a potent stressor and produces persistent dysregulation of brain reward systems, including the VTA, as well as stress/anti-stress responsivity (Becker, 2017).…”