CSF Levels of Norepinephrine During Alcohol Withdrawal

Rj, Hawley; Lf, Major; Ea, Schulman; Lake, C. Raymond

doi:10.1001/archneur.1981.00510050055008

Cited by 57 publications

(20 citation statements)

References 30 publications

(1 reference statement)

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“…Hyperactive norepinephrine signaling is thought to be a core feature of the pathophysiology of PTSD (Bremner et al, 1997;Yehuda et al, 1998;Geracioti et al, 2001;Pietrzak et al, 2013;Steuwe et al, 2014). It may also be involved in SUD, as human and animal studies have found elevations in both central and peripheral noradrenergic activity during all phases of substance use including acute intoxication, chronic use, withdrawal, and relapse (Hawley et al, 1981;Kovács et al, 2002;Patkar et al, 2003;Lanteri et al, 2008;Fitzgerald, 2013). This might suggest that blockade of excessive noradrenergic activity would be helpful for both SUD and PTSD.…”

Section: Overlapping Effects Of Trauma and Drugs On Neuronal And Endomentioning

confidence: 99%

Mechanisms of Shared Vulnerability to Post-traumatic Stress Disorder and Substance Use Disorders

Maria-Rios

Morrow

2020

Front. Behav. Neurosci.

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Psychoactive substance use is a nearly universal human behavior, but a significant minority of people who use addictive substances will go on to develop an addictive disorder. Similarly, though ∼90% of people experience traumatic events in their lifetime, only ∼10% ever develop post-traumatic stress disorder (PTSD). Substance use disorders (SUD) and PTSD are highly comorbid, occurring in the same individual far more often than would be predicted by chance given the respective prevalence of each disorder. Some possible reasons that have been proposed for the relationship between PTSD and SUD are self-medication of anxiety with drugs or alcohol, increased exposure to traumatic events due to activities involved in acquiring illegal substances, or addictive substances altering the brain's stress response systems to make users more vulnerable to PTSD. Yet another possibility is that some people have an intrinsic vulnerability that predisposes them to both PTSD and SUD. In this review, we integrate clinical and animal data to explore these possible etiological links between SUD and PTSD, with an emphasis on interactions between dopaminergic, adrenocorticotropic, GABAergic, and glutamatergic neurobehavioral mechanisms that underlie different emotional learning styles.

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Section: Overlapping Effects Of Trauma and Drugs On Neuronal And Endomentioning

confidence: 99%

Mechanisms of Shared Vulnerability to Post-traumatic Stress Disorder and Substance Use Disorders

Maria-Rios

Morrow

2020

Front. Behav. Neurosci.

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“…Disrupted noradrenergic signaling has long been implicated in excessive alcohol intake. Alcohol acutely increases plasma NE in non-dependent humans (Howes & Reid, 1985) and mice (Hawley, Major, Schulman, & Lake, 1981; Kovacs, Soroncz, & Tegyei, 2002), and NE depletion may reduce the rewarding effects of alcohol intake (Ventura, De Carolis, Alcaro, & Puglisi-Allegra, 2006). Interestingly, there is some evidence that alcohol withdrawal increases NE levels (Kovacs et al, 2002), and noradrenergic therapeutics that decrease LC excitability have shown some efficacy in reducing drinking and the negative symptoms of alcohol withdrawal in clinical populations (Muzyk, Fowler, Norwood, & Chilipko, 2011; Simpson et al, 2009) as well as in preclinical models of excessive alcohol drinking (Gilpin & Koob, 2010; Le, Harding, Juzytsch, Funk, & Shaham, 2005; Skelly & Weiner, 2014; B.…”

Section: ) Critical Extrahypothalamic Sites For Crf Signaling: Bnst mentioning

confidence: 99%

CRF modulation of central monoaminergic function: Implications for sex differences in alcohol drinking and anxiety

Pleil

Skelly

2018

Alcohol

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Decades of research have described the importance of corticotropin-releasing factor (CRF) signaling in alcohol addiction, as well as in commonly co-expressed neuropsychiatric diseases, including anxiety and mood disorders. However, CRF signaling can also acutely regulate binge alcohol consumption, anxiety, and affect in non-dependent animals, possibly via modulation of central monoaminergic signaling. We hypothesize that basal CRF tone is particularly high in animals and humans with an inherent propensity for high anxiety and alcohol consumption, and thus these individuals are at increased risk for the development of alcohol use disorder and comorbid neuropsychiatric diseases. The current review focuses on extrahypothalamic CRF circuits, particularly those stemming from the bed nucleus of the stria terminalis (BNST), found to play a role in basal phenotypes, and examines whether the intrinsic hyperactivity of these circuits is sufficient to escalate the expression of these behaviors and steepen the trajectory of development of disease states. We focus our efforts on describing CRF modulation of biogenic amine neuron populations that have widespread projections to the forebrain to modulate behaviors, including alcohol and drug intake, stress reactivity, and anxiety. Further, we review the known sex differences and estradiol modulation of these neuron populations and CRF signaling at their synapses to address the question of whether females are more susceptible to the development of comorbid addiction and stress-related neuropsychiatric diseases because of hyperactive extrahypothalamic CRF circuits compared to males.

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“…Proposed mechanisms posit that noradrenergic neurons in pre-frontal cortex project caudally to the ventral tegmental area and promote dopamine release into the nucleus accumbens (Ventura et al, 2003) and that norepinephrine, acting via α 1 -adrenergic receptors located pre-synaptically on dopaminergic neurons projecting to nucleus accumbens, directly drives dopamine release in that location (Mitrano et al, 2012). Norepinephrine levels in the periphery and in the central nervous system are elevated in animals and humans during alcohol withdrawal (Hawley et al, 1981; Kovacs et al, 2002; Patkar et al, 2003), and elevated norepinephrine levels in the extended amygdala are proposed to play a role in stress-induced relapse (Kash, 2012; Koob, 2009). …”

Section: Noradrenergic Brain Systems Are Implicated In Both Aud and Ptsdmentioning

confidence: 99%

A Pilot Trial of Prazosin, an Alpha‐1 Adrenergic Antagonist, for Comorbid Alcohol Dependence and Posttraumatic Stress Disorder

Simpson

Malte

Dietel

et al. 2015

Alcoholism Clin & Exp Res

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Background Posttraumatic Stress Disorder (PTSD) and alcohol dependence (AD) commonly co-occur and are associated with greater symptom severity and costs than either disorder alone. No pharmacologic interventions have been found to decrease both alcohol use and PTSD symptom severity relative to matched placebo. Prazosin, an alpha-1 adrenoreceptor antagonist, has demonstrated efficacy reducing PTSD and AD symptoms among individuals with one or the other disorder and may be useful in addressing comorbid PTSD/AD. Methods Prazosin and matched placebo were compared in the context of an outpatient 6-week double-blind randomized controlled pilot trial involving 30 individuals with comorbid PTSD/AD. Medication was titrated to 4mg q AM, 4mg q PM and 8mg qhs by the end of week 2. Participants in both conditions received five Medical Management sessions. Information regarding alcohol use, craving, and PTSD was gathered daily using a telephone Interactive Voice Response (IVR) system. Results Participants randomized to prazosin had a greater reduction in percent days drinking per week and percent days heavy drinking per week between baseline and week 6 than did placebo participants. No significant differences were detected within or between groups in change from weeks 1 to 6 in total PTSD symptoms. Participants in the prazosin condition reported drowsiness on significantly more days than those in the placebo condition. Conclusions Consistent with the extant research evaluating medications for comorbid PTSD/AD, the current evaluation of prazosin also found decreased alcohol consumption but no medication effect on PTSD symptomatology.

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CSF Levels of Norepinephrine During Alcohol Withdrawal

Cited by 57 publications

References 30 publications

Mechanisms of Shared Vulnerability to Post-traumatic Stress Disorder and Substance Use Disorders

Mechanisms of Shared Vulnerability to Post-traumatic Stress Disorder and Substance Use Disorders

CRF modulation of central monoaminergic function: Implications for sex differences in alcohol drinking and anxiety

A Pilot Trial of Prazosin, an Alpha‐1 Adrenergic Antagonist, for Comorbid Alcohol Dependence and Posttraumatic Stress Disorder

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