Chronic daily ethanol and withdrawal: 6. Effects on rat sympathoadrenal activity during “abstinence”

Rasmussen, Dennis D.; Wilkinson, Charles W.; Raskind, Murray A.

doi:10.1016/j.alcohol.2006.06.007

Cited by 36 publications

(30 citation statements)

References 33 publications

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“…Although sympathetic activation is increased during alcohol deprivation in rats and humans (Ehrenreich et al, 1997;Patkar et al, 2004;Rasmussen et al, 2006) and excessive brain and peripheral noradrenergic activation are associated with increased anxiety (Sullivan et al, 1999), it remains to be determined how acutely blocking noradrenergic signaling (including potential interactions between noradrenergic and CRF signaling) at the time of stress suppresses anxiety-like behavior during a subsequent alcohol deprivation 7 days later. It has been demonstrated that administrations of corticosterone instead of stress do not decrease subsequent alcohol deprivation-induced anxiety in this model (Breese et al, 2004), so it is unlikely that prazosin effects on corticosterone secretion play an important mediating role.…”

Section: Discussionmentioning

confidence: 99%

Prazosin Prevents Increased Anxiety Behavior That Occurs in Response to Stress During Alcohol Deprivations

Rasmussen

Kincaid

Froehlich

2016

Alcohol and Alcoholism

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Aims: Stress-induced anxiety is a risk factor for relapse to alcohol drinking. The aim of this study was to test the hypothesis that the central nervous system (CNS)-active α 1 -adrenergic receptor antagonist, prazosin, would block the stress-induced increase in anxiety that occurs during alcohol deprivations. Methods: Selectively bred male alcohol-preferring (P) rats were given three cycles of 5 days of ad libitum voluntary alcohol drinking interrupted by 2 days of alcohol deprivation, with or without 1 h of restraint stress 4 h after the start of each of the first two alcohol deprivation cycles. Prazosin (1.0 or 1.5 mg/kg, IP) or vehicle was administered before each restraint stress. Anxiety-like behavior during alcohol deprivation following the third 5-day cycle of alcohol drinking (7 days after the most recent restraint stress ± prazosin treatment) was measured by performance in an elevated plus-maze and in social approach/avoidance testing. Results: Rats that received constant alcohol access, or alcohol access and deprivations without stress or prazosin treatments in the first two alcohol deprivations did not exhibit augmented anxiety-like behavior during the third deprivation. In contrast, rats that had been stressed during the first two alcohol deprivations exhibited increased anxiety-like behavior (compared with control rats) in both anxiety tests during the third deprivation. Prazosin given before stresses in the first two cycles of alcohol withdrawal prevented increased anxiety-like behavior during the third alcohol deprivation. Conclusion: Prazosin treatment before stresses experienced during alcohol deprivations may prevent the increased anxiety during subsequent deprivation/abstinence that is a risk factor for relapse to alcohol drinking. Short summary: Administration of prazosin before stresses during repetitive alcohol deprivations in male alcohol-preferring (P) rats prevents increased anxiety during a subsequent deprivation without further prazosin treatment. Prazosin treatment during repeated alcohol deprivations may prevent the increased anxiety that is a risk factor for relapse to alcohol drinking.

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Section: Discussionmentioning

confidence: 99%

Prazosin Prevents Increased Anxiety Behavior That Occurs in Response to Stress During Alcohol Deprivations

Rasmussen

Kincaid

Froehlich

2016

Alcohol and Alcoholism

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“…Alterations in HPA axis responses have been observed during active drinking, acute withdrawal, and 4 weeks postwithdrawal from alcohol (Wand and Dobs, 1991;Adinoff et al, 1991Adinoff et al, , 2005Koob et al, 2004). Furthermore, autonomic dysregulation has been noted during acute alcohol withdrawal, and altered cardiovascular and noradrenergic responsivity has been seen during the protracted alcohol abstinence period (Krystal et al, 1996;Bernardy et al, 2003;Rasmussen et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Enhanced Negative Emotion and Alcohol Craving, and Altered Physiological Responses Following Stress and Cue Exposure in Alcohol Dependent Individuals

Sinha

Fox

Hong

et al. 2008

Neuropsychopharmacol

409

383

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Chronic alcohol abuse is associated with changes in stress and reward pathways that could alter vulnerability to emotional stress and alcohol craving. This study examines whether chronic alcohol abuse is associated with altered stress and alcohol craving responses. Treatment-engaged, 28-day abstinent alcohol-dependent individuals (ADs; 6F/22M), and social drinkers (SDs; 10F/18M) were exposed to a brief guided imagery of a personalized stressful, alcohol-related and neutral-relaxing situation, one imagery condition per session, presented in random order across 3 days. Alcohol craving, anxiety and emotion ratings, behavioral distress responses, heart rate, blood pressure, and salivary cortisol measures were assessed. Alcohol patients showed significantly elevated basal heart rate and salivary cortisol levels. Stress and alcohol cue exposure each produced a significantly enhanced and persistent craving state in alcohol patients that was marked by increased anxiety, negative emotion, systolic blood pressure responses, and, in the case of alcohol cue, behavioral distress responses, as compared to SDs. Blunted stress-induced cortisol responses were observed in the AD compared to the SD group. These data are the first to document that stress and cue exposure induce a persistent negative emotion-related alcohol craving state in abstinent alcoholics accompanied by dysregulated HPA and physiological arousal responses. As laboratory models of stress and negative mood-induced alcohol craving are predictive of relapse outcomes, one implication of the current data is that treatments targeting decreases in stress and alcohol cue-induced craving and regulation of stress responses could be of benefit in improving alcohol relapse outcomes.

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“…For example, using animal models of drug self-administration and reinstatement, preclinical studies have shown CRF antagonists and α-2-adrenergic agonists to be efficacious in reducing stress-related drug seeking in addicted laboratory animals (see Shaham et al 2003;Weiss 2005 for review). Similarly, α1-adrenergic antagonists such as Prazosin have been found to decrease alcohol withdrawal symptoms, alcohol consumption and stress-induced relapse in animal models (Gilpin et al 2009;Rasmussen et al 2006;Walker et al 2008) and in a pilot clinical study of alcoholics (Simpson et al 2009). …”

Section: Related Relapsementioning

confidence: 99%

Modeling Relapse Situations in the Human Laboratory

Sinha

2011

Current Topics in Behavioral Neurosciences

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It is well known that alcoholism is a chronic relapsing illness. While stress significantly impacts alcoholism risk, there is also evidence that increasing levels of alcohol use affect peripheral and central stress and reward pathways thereby setting up a reciprocal relationship among the effects of alcohol consumption of the development, course of and recovery from alcoholism. This chapter reviews our efforts in assessing the integrity of stress pathways in alcoholism by examining whether altered responses of the stress pathways play a role in relapse risk. Using validated human laboratory procedures to model two of the most common situations that contribute to relapse risk, we review how such models in the laboratory can predict subsequent alcohol relapse. Empirical findings from human laboratory and brain imaging studies are reviewed to show that specific stress-related dysregulation accompanies the alcohol craving state in alcohol-dependent individuals, and such dysregulation along with increases in alcohol seeking are predictive of increased alcohol relapse risk. Finally, the significant implications of these findings for the development of novel treatment interventions that target stress processes and alcohol craving to improve alcoholism relapse outcomes are discussed.

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Chronic daily ethanol and withdrawal: 6. Effects on rat sympathoadrenal activity during “abstinence”

Cited by 36 publications

References 33 publications

Prazosin Prevents Increased Anxiety Behavior That Occurs in Response to Stress During Alcohol Deprivations

Prazosin Prevents Increased Anxiety Behavior That Occurs in Response to Stress During Alcohol Deprivations

Enhanced Negative Emotion and Alcohol Craving, and Altered Physiological Responses Following Stress and Cue Exposure in Alcohol Dependent Individuals

Modeling Relapse Situations in the Human Laboratory

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