Cerebrospinal Fluid 3-Methoxy-4-hydroxyphenylglycol and Norepinephrine Levels in Alcohol Withdrawal

Hawley, Rollin J.

doi:10.1001/archpsyc.1985.01790340034005

Cited by 109 publications

(19 citation statements)

References 42 publications

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“…We thus wanted to examine if stressful manipulations, which would increase adrenergic tone in vivo, could alter the expression of α 1 -AR LTD ex vivo. Withdrawal from alcohol intoxication has been shown to increase anxiety (40), and patients experiencing withdrawal have elevated levels of NE and its metabolites (36,41). Furthermore, CIE can increase anxiety-like behavior in animal models (44).…”

Section: Discussionmentioning

confidence: 99%

Distinct forms of G _q -receptor-dependent plasticity of excitatory transmission in the BNST are differentially affected by stress

McElligott

Klug

Nobis

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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Long-term depression (LTD) is an important synaptic mechanism for limiting excitatory influence over circuits subserving cognitive and emotional behavior. A major means of LTD induction is through the recruitment of signaling via G q -linked receptors activated by norepinephrine (NE), acetylcholine, and glutamate. Receptors from these transmitter families have been proposed to converge on a common postsynaptic LTD maintenance mechanism, such that hetero-and homosynaptic induction produce similar alterations in glutamate synapse efficacy. We report that in the dorsolateral and ventrolateral bed nucleus of the stria terminalis (BNST), recruitment of G q -linked receptors by glutamate or NE initiates mechanistically distinct forms of postsynaptically maintained LTD and these LTDs are differentially regulated by stress exposure. In particular, we show that although both mGluR5-and α 1 -adrenergic receptor (AR)-dependent LTDs involve postsynaptic endocytosis, the α 1 -AR-initiated LTD exclusively involves modulation of signaling through calcium-permeable AMPA receptors. Further, α 1 -AR-but not mGluR5-dependent LTD is disrupted by restraint stress. α 1 -AR LTD is also impaired in mice chronically exposed to ethanol. These data thus suggest that in the BNST, NE-and glutamate-activated G q -linked signaling pathways differentially tune glutamate synapse efficacy in response to stress.addiction | norepinephrine | metabotropic glutamate receptor | calcium-permeable AMPA receptor | ethanol A lterations in key amygdalar and reward circuitries have been proposed as potential mechanisms underlying interrelated anxiety disorders and addiction. The bed nucleus of the stria terminalis (BNST) is a nucleus within a series of structures known as the "extended amygdala," which receives a mix of glutamatergic inputs from cognitive and systemic brain centers and projects to key nuclei in both the reward and stress circuitries (1, 2). Consistent with this anatomy, a large literature indicates key roles of this region in anxiety-related behaviors, addiction, and other affective disorders (3).The BNST receives intense noradrenergic innervation through the ventral noradrenergic bundle (VNAB) (4). Disruption of the VNAB or noradrenergic signaling in the BNST alters responses to stressors, preference for opiates, and stress-induced reinstatement to drug seeking (5, 6). α 1 -Adrenergic receptors (ARs) are G qlinked G-protein-coupled receptors (GPCRs) that participate in shaping responses to stressors. Signaling through BNST α 1 -ARs within the BNST potently regulates the hypothalamic-pituitaryadrenal (HPA) stress axis and anxiety responses after stressors (7). The α 1 -AR antagonist prazosin has been shown to attenuate ethanol self-administration (SA) in ethanol-dependent rats (8) and reduces opiate SA (9). Furthermore, data from clinical trials have demonstrated that prazosin alleviates symptoms of posttraumatic stress disorder (PTSD) (10) and reduces alcohol drinking behavior in alcoholics (11).Like α 1 -ARs, group I metabotropic glutamat...

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Section: Discussionmentioning

confidence: 99%

Distinct forms of G _q -receptor-dependent plasticity of excitatory transmission in the BNST are differentially affected by stress

McElligott

Klug

Nobis

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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“…Through repeated cycles of binge consumption and withdrawal, there are significant increases in neuroendocrine tolerance and basal state autonomic upregulation (Breese et al, 2011; Sinha et al, 2011). Specifically, acute withdrawal states are associated with increases in CRF levels in cerebrospinal fluid and blood plasma levels of ACTH, cortisol, norepinephrine, and epinephrine (Breese et al, 2011; D’Sa et al, 2012; Hawley et al, 1985; Heilig et al, 2010; Markus et al, 2002). In addition, in several previous studies by our group, we have shown that early abstinence up to 4 weeks is associated with continued high basal ACTH and cortisol as well as higher basal heart rates, and blunted or suppressed ACTH, cortisol, and heart rate responses to pharmacological and psychological challenges in alcohol dependent individuals (Fox et al, 2012a; Fox et al, 2008; Sinha, 2012; Sinha et al, 2012; Sinha et al, 2011a; Sinha et al, 2009b).…”

Section: Hpa Axis and Prefrontal Dysregulation Increase Cue Reactimentioning

confidence: 99%

Alcohol, stress, and glucocorticoids: From risk to dependence and relapse in alcohol use disorders

2017

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In this review, we detail the clinical evidence supporting the role of psychological and physiological stress in instrumental motivation for alcohol consumption during the development of mild to moderate alcohol use disorders (AUDs) and in the compulsive, habitual alcohol consumption seen in severe, chronic, relapsing AUDs. Traditionally, the study of AUDs has focused on the direct and indirect effects of alcohol on striatal dopaminergic pathways and their role in the reinforcing effects of alcohol. However, growing evidence also suggests that alcohol directly stimulates the hypothalamic pituitary adrenal (HPA) axis and has effects on glucocorticoid receptors in extrahypothalamic, limbic forebrain, and medial Prefrontal Cortex (PFC) circuits, which contribute to the development of AUDs and their progression in severity, chronicity, and relapse risk. Evidence indicates HPA axis, glucocorticoid, and PFC dysfunction during protracted withdrawal and under high arousal conditions in those with severe AUDs, and novel evidence is also emerging to suggest HPA axis dysfunction with binge/heavy drinking, which is associated with motivation for alcohol in non-dependent individuals. Specifically, alcohol-associated alterations in HPA axis responses to stress and alcohol cues may serve as interoceptive physiological signals and facilitate conditioning mechanisms to influence alcohol motivation. Thus, this dysfunction may serve as a potential biomarker of both risk and of relapse. Based on this emerging data, we conceptualize and present early evidence for treatment targets that may improve PFC function and/or normalize HPA axis functioning and may be beneficial in the treatment and relapse prevention of AUDs. Finally, we suggest that individual differences in alcohol-related pathophysiology in these circuits may modulate treatment and recovery response, thereby supporting the need for building personalized medicine algorithms to understand and treat AUDs.

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“…30 Fourth, alcohol dependence, as well as sleep deprivation, are thought to increase catecholamine release through activation of central nervous system centers and alterations of sympathovagal balance. 11,2741,42 Alcoholic subjects who have a night of insufficient sleep may be particularly vulnerable to increases of blood pressure and heart rate in the morning. 11,12 Cardiovascular events are known to occur more frequently from early morning to noon, 14 and longitudinal studies have found that autonomic dysregulation is related to greater risk of cardiovascular disease.…”

Section: Irwin and Ziegler Sleep Deprivation And Sympathetic Activatimentioning

confidence: 99%

Sleep Deprivation Potentiates Activation of Cardiovascular and Catecholamine Responses in Abstinent Alcoholics

Irwin

2005

Hypertension

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Abstract-Alcohol dependence is associated with an increased incidence of hypertension and cardiac arrhythmias, but the triggering mechanisms are not known. Sleep loss, common in alcohol-dependent patients, causes an activation of the sympathetic nervous system. To determine whether sleep deprivation induces differential cardiovascular and sympathetic responses in alcohol dependence, we measured heart rate, blood pressure, and circulating sympathetic catecholamines in 36 abstinent alcohol-dependent men and 36 age-, gender-, and ethnicity-matched controls after a baseline night of sleep, in the morning after early night partial sleep deprivation, and again after a full night of recovery sleep. Subjects were on average normotensive and none was being treated for hypertension. Baseline heart rate, blood pressure, and sympathetic catecholamines were similar in the 2 groups. Administration of partial night sleep deprivation induced greater increases of heart rate (PϽ0.01) and circulating levels of norepinephrine (PϽ0.05) and epinephrine (PϽ0.05) in the alcohol-dependent men as compared with responses in controls. Even after a full night of recovery sleep, elevations in heart rate (PϽ0.05) and circulating catecholamines (PϽ0.05) persisted in the alcoholic subjects. Partial night sleep deprivation induces elevated heart rate and sympathetic catecholamine responses in alcoholic subjects as compared with controls, and this sympathetic activation is sustained after nights of partial and recovery sleep. A lcohol dependence, which exceeds a lifetime incidence of 10%, 1 is a major risk factor for cardiovascular diseases, with alcohol-dependent men showing an increased prevalence of hypertension and cardiac arrhythmias. 2,3 An increase of sympathetic nervous system activity is implicated as being one underlying mechanism of the deleterious cardiovascular effects of chronic alcohol consumption. 4 Human studies have found that acute alcohol intake induces elevations of heart rate and blood pressure via centrally mediated increases of sympathetic discharge. 5 There is also evidence that abnormalities of cardiovascular regulation persist into recovery. Abstinent alcohol-dependent male patients show exaggerated heart rate and blood pressure reactivity in response to behavioral stress, although measures of sympathetic activation have not been determined. 6 -8 In this study, we examined cardiovascular responses and circulating levels of norepinephrine and epinephrine at rest and in response to a behavioral challenge, sleep deprivation, in abstinent male alcohol-dependent patients.Experimental sleep deprivation can serve as a naturalistic probe of the homeostatic regulation of sympathetic activity. Loss of sleep induces elevations in circulating levels of epinephrine and norepinephrine, 9,10 with attendant increases of blood pressure and heart rate the next day. 11,12 In addition, habitual sleep loss and insomnia are markers of subclinical heart disease and are independent predictors of cardiovascular disease risk, particularly in ma...

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Cerebrospinal Fluid 3-Methoxy-4-hydroxyphenylglycol and Norepinephrine Levels in Alcohol Withdrawal

Cited by 109 publications

References 42 publications

Distinct forms of G _q -receptor-dependent plasticity of excitatory transmission in the BNST are differentially affected by stress

Distinct forms of G _q -receptor-dependent plasticity of excitatory transmission in the BNST are differentially affected by stress

Alcohol, stress, and glucocorticoids: From risk to dependence and relapse in alcohol use disorders

Sleep Deprivation Potentiates Activation of Cardiovascular and Catecholamine Responses in Abstinent Alcoholics

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Cerebrospinal Fluid 3-Methoxy-4-hydroxyphenylglycol and Norepinephrine Levels in Alcohol Withdrawal

Cited by 109 publications

References 42 publications

Distinct forms of G q -receptor-dependent plasticity of excitatory transmission in the BNST are differentially affected by stress

Distinct forms of G q -receptor-dependent plasticity of excitatory transmission in the BNST are differentially affected by stress

Alcohol, stress, and glucocorticoids: From risk to dependence and relapse in alcohol use disorders

Sleep Deprivation Potentiates Activation of Cardiovascular and Catecholamine Responses in Abstinent Alcoholics

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Product

Resources

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Distinct forms of G _q -receptor-dependent plasticity of excitatory transmission in the BNST are differentially affected by stress

Distinct forms of G _q -receptor-dependent plasticity of excitatory transmission in the BNST are differentially affected by stress